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Interstitial  Gingivitis 


SO-CALLED  PYORRHiEA  ALVEOLARIS 


EUGENE  S.  TALBOT,  M.  D.,  D.  D.  S. 

Professor  of  Dental  and  Oral  Sdrgery,  Northwestern  University.  Woman's  Medical  School 
Honorary  President  of  the  Dental  Section  of  the  Tenth  International  Medical  Congress, 
Berlin,  1890;  Honorary  President  of  the  Dental  Section  of  the  Twelfth  International 
Medical  Congress,  Moscow,  1897;  Honorary  Secretary   of  the  Pan-American  Medical 
Congress,  Washington,  1893;  Member  of  the  American  Medical  Assoclation;  Fellow 
OF  the  Chicago  Academy  of  Medicine;  Member  of  the  Chicago  Medical  Society; 
Secretary  of  the  Section  on  Stomatology  of  the  American  Medical  Asso- 
ciation; Member  of  the  Chicago  Academy  of  Sciences;  Honorary  Member 
OF   THE   Odontologischen   Gesellschaft.    Berlin,    Germany;    Membre 
Honoraire  de  l'Association   Generale   des   Dentistes  de   France; 
Honorary  Member  Sociedad  Odontologia  Espanola;   Author  of 
"The  Irregularities  of  the  Teeth  and  their  Treatment" 
Author  of  "  Chart  of  Typical  Forms  of  Constitutional 
Irregularities  of  the  Teeth";  Author  of  "The  Eti- 
ology OF  Osseous  Deformities  of  the  Head,  Face, 
Jaws  and  Teeth";  Author  of  "  Degeneracy,  its 
Causes,   Signs   and   Results  ";    Etc.,    Etc. 


WITH   SEVENTV-THREE    ILLUSTRATIONS. 


PiriLADELPHIA  : 

AVIIITE   DENTAL   MA.NT  FACT  L'HING   CO. 
ISili). 


Entered  According  to  Act  of  Congress,  in  the  Year  1899,  by 

Eugene  S.  Talbot, 

1  the  Office  of  tbe  Librarian  of  Congress  at  Washington,  D.  C. 


T  K 


ALL  CO-WOEKERS  IN  DENTAL  SCIENCE, 

This  Work, 

As  a  Slight  Tolcen  of  Appreciation  of  Their  Contributions  to  Science, 

is  Respectfully  Dedicated. 


PREFACE. 


The  great  law  of  medical  science,  that  to  know  the  cause  is 
half  the  treatment,  is  as  applicable  to  dentistry  as  to  any  other 
specialty  of  medicine,  and  is  as  aj^plicable  to  dental  problems  as 
to  those  of  biology  generally.  Treatment  of  any  disease  without 
knowledge  of  its  pathology  is  practically  a  failure. 

While  much  has  been  written  upon  the  pyorrhoeic  stage  of 
interstitial  gingivitis  ami  its  treatment,  during  the  past  tw(_) 
decades,  no  new  principle  has  been  advanced  whereby  the  jmrts 
can  be  restored  to  a  healthy  condition,  or  whereby  the  disease 
can  be  prevented.  The  disease  is  admittedly  on  the  increase. 
This  seems  at  first  sight  to  indicate  that  dental  projjhylaxis  and 
treatment,  so  far  as  this  disease  is  concerned,  is  a  failure. 

Other  specialists  restore  jjatients  to  health.  Nearly  every 
j)atient  with  this  disease  applies  to  dentists.  Most  dentists,  how- 
ever, hardly  knoAV  the  disease  exists  and  much  less  are  capable 
of  offering  suggestions  as  to  treatment.  It  seems  strange  that  in 
America  so  little  original  woi'k  has  been  done  ujion  a  disease 
more  to  be  dreaded  than  tooth  decay.  Treatment  has  been 
wholly  at  random,  and  hence,  as  a  rule,  only  to  limited  extent 
successful.  Destruction  of  the  alveolar  process  and  loss  of  the 
teeth  is  so  rapidly  sure  that  the  necessity  for  dental  scientists  to 
solve  the  etiology  of  this  very  common  disease  seems  imperative. 

Nearly  two  decades  ago  I  felt  and  expressed  the  necessity  for 
more  extended  study  (Dental  Cosmos,  1886,  page  689)  of  the 
clinical  aspects  and  etiology  of  this  disease.  Even  during  appar- 
ently diverse  and  sej)arated  studies,  such  as  those  related  to  dental 
and  maxillary  irregularities  and  degeneracy,  the  necessity  for 
this  has  forced  itself  still  further  upon  me.  In  the  present 
study,  the  disease  has,  of  necessity,  been  considered  from  the 
broad  standpoint  of  general  pathology.  In  all  instances  where 
possible  personal  elements  of  error  are  present,  these  have  been 
eliminated  bv  having  researches  made  bv  more  than  one  observer. 


The  attempt  has  been  made  to  summarize  all  researches  on 
the  subject.  So  much  have  opinions  been  intermingled  that  it  is 
possible  that  proper  credit  for  priority  has  unintentionally  not 
been  given. 

The  author  is  under  obligation  to  the  following  scientists  for 
their  kind  assistance :  Dr.  Ludwig  Hektoen,  Pathologist,  Rush 
Medical  College ;  Dr.  Jerome  H.  Salisbury,  Chemist,  Rush 
Medical  College  ;  Dr.  W.  A.  Evans,  Pathologist,  Columbus  Med- 
ical Laboratory,  Professor  of  Pathology,  Chicago  College  of 
Physicians  and  Surgeons  and  Milwaukee  Medical  College ;  Dr. 
J.  A.  Wesener,  Chemist,  Columbus  Medical  Laboratory,  Profes- 
sor of  Chemistry,  Chicago  College  of  Physicians  and  Surgeons ; 
Dr.  Vida  A.  Latham,  Pathologist,  Northwestern  University, 
Woman's  Medical  School;  Dr.  Maximilian  Herzog,  Pathologist, 
Chicago  Polyclinic  Hospital ;  Professor  Theo.  A.  Edwin  Klebs 
and  Dr.  Robert  F.  Zeit,  Pathologists,  and  Dr.  W.  L.  Baum, 
Professor  of  Diseases  of  the  Skin,  Post-Graduate  Medical  School, 
Chicago ;  Dr.  G.  V.  I.  Brown,  Professor  of  Oral  Surgery,  Dental 
Department,  Milwaukee  Medical  College ;  Dr.  Frederick  Noyes, 
Histologist,  Dental  Department,  Northwestern  University ;  Dr. 
J.  G.  Kiernan,  and  to  Blomgren  Bros.  &  Co.  for  electrotyjoes,  etc. 

THE  AUTHOR. 

103  State  Street,  Chicago. 


CONTENTS. 


I.    History  .........        1 

II.      iNTRODUC'flON  .  .  .  .  .  .  .      ■        .  10 

III.  Tr.^nsitory  Structures  — 

The  Jaws 20 

The  Alveolar  Process  21 
Periosteum  and  Peridental  Me.mbrane       .          .          .  33 
The  Gums  and  Mucous  Membrane             ...  42 
Do  Glands  Exist  in  Epithelial  and  Peridental  Mem- 
brane?          .......  -47 

Bone  Building  and  Absorption        ....  59 

IV.  Theories  of  Interstitial  Gingivitis            .          .          .          .65 
V.    Uric  Acid  and  Interstitial  Gingivitis            ...  68 

VI.  Inorganic  Salts  and  Interstitial  Gingivitis      .          .  .73 

VII.  Heredity  and  Environment            .....  83 

VIII.  Degeneracy  and  Degenerate  Tissues         .          .          .  .86 

IX.  Neurotic,   Diathetic  and  Degenerate  Children    .          .  89 

X.  Interstitial  Gingivitis  in  Dogs          .          .          .          .  .98 

XL  Mercurial  Interstitial  Gingivitis  in  Dogs             .          .  117 

XII.  Bacteriology  of  Interstitial  Gingivitis             .          .  .122 

XIII.  Scorbutic  Interstitial  Gingivitis  in  Man     .          .          .  127 

XIV.  Interstitial  Gingivitis  in  Man  fro.m  Metallic  and  Other 

Drug  Action       ........    142 

XV.    Conclusions  .  .  .    •      .  .  .  .  .         146 

Pathogenesis  of  Interstiti.vl  Gingivitis     .  .  .151 

Endarteritis  Obliterans         .  .  .  .  .154 

Absorption  of  the  Alveolar  Process  .  .  .    157 

Pyorrhoea  Alveolaris  from  Interstitial  Gingivitis    .    162 
Constitutional  Effects  op  Pyorrhea  Alveolaris  .         167 
Calcic  Deposits  .  .  .  .  .  .  .168 

XVI.    Treatment    .  .  .  .  .  .  .  .  .172 


INTERSTITIAL  GINGIVITIS. 


CHAPTER    I. 

HISTORY. 

Inflammation  of  the  peridental  membrane  is  probal)!}''  coeval 
with  man.  Some  of  the  skulls  found  earliest  in  the  cave-dwell- 
ing period  exhibit  evidences  of  its  j)resence.  In  some  of  these, 
careful  observation  has  shown  deposits  encroaching  npon  the 
roots  of  the  teeth  and  resultant  absorption  of  the  alveolar 
process. 

In  the  Swiss  lake-dwellings  and  in  the  earlier  Irish  cran- 
noges  of  like  construction  and  situation,  skulls  are  found,  which 
exhibit  deposits  of  tartar,  inflammation  of  the  peridental  mem- 
brane and  absorj)tion  of  the  alveolar  process.  These  skulls  were 
those  of  primitive  races  in  whom  disease  of  the  jaws  and  teeth  is 
supposed  to  be  absent  or  infrequent.  In  the  skulls  of  the  peo- 
ples exhibiting  the  highest  civilization  at  the  earliest  ]3eriod  — 
those  of  the  Accadians  and  EgyjDtians  —  similar  inflammatory 
conditions  are  to  be  found.  This,  however,  was  to  have  been 
expected,  to  judge  from  the  dental  directions  left  among  the 
medical  records  of  these  i^eoples.  The  Greeks,  Syrians,  Arab- 
ians, Dravidians  and  Aryans  of  India  and  the  early  Burmese 
all  suffered  from  this  disorder.  In  the  museum  at  Constan- 
tinojjle  are  the  skulls  of  soldiers  who  fought  at  a  battle  328 
B.  C.  One  of  these  skulls  has  the  anterior  alveolar  process 
entirely  absorbed  away.  The  roots  of  the  right  central,  the 
right  lateral  and  the  left  central  incisors  are  exposed. 

Inflammation  of  the  peridental  membranes,  it  will  be  evident, 
is,  therefore,  not  a  modern  disease ;  not  a  disease  confined  either 
to  civilized  or  primitive  races,  but  one  which  attacked  man  early 


I  INTERSTITIAL    GINGIVITIS. 

in  his  evolution.  Like  most  diseases  it  has  been  chiefly  dis- 
cussed and  analyzed  during  the  past  two  centuries. 

In  1740  H.  A.  Fauchard '  (while  recognizing  the  disease  in 
all  its  essential  features  and  describing  its  principal  symptoms) 
advanced  no  theory  as  to  its  origin. 

In  1778  M.  Jourdain "  advanced  the  opinion  that  the  disease 
was  of  scorbutic  origin. 

In  1821  L.  Kaecker  ^  discussed  the  disorder  in  an  essay  on 
the  devastations  of  the  gums  and  alveolar  processes. 

In  1822  M.  Joirac*  (in  a  discussion  of  the  disease),  Avhile 
advancing  no  theory  as  to  its  origin,  called  it  "  pyorrhoea  inter- 
alveolo-dentaire. " 

In  1860  Marshall  de  Calve  ^  advanced  the  opinion  that  the 
disorder  was  of  hereditary  origin. 

In  1867  Magitot,  discussing  the  disorder,  advanced  the 
opinion  that  the  gum,  being  in  all  cases  only  attacked  subse- 
quently, is  not  the  original  seat  of  the  lesion.  In  his  ojiinion 
systemic  disorders  like  gout,  rheumatism,  albuminuria,  diabetes 
and  anaemia  had  an  influence. 

BonwilP  during  the  same  year  exjjressed  the  oj^inion  that 
the  disorder  was  due  to  thinness  of  the  alveolar  process  between 
the  teeth,  thus  depriving  the  peridental  membrane  and  gum 
tissue  of  proper  support.  The  want  of  proper  articulation  of 
the  teeth  also  exerted  an  influence. 

In  1870  Brown  ascribed  the  disorder  to  serumal  calculus. 

In  1875  John  T.  Riggs,  after  whom  the  disorder  is  frequently 
called,  entitled  it  (in  a  paper  read  before  the  American 
Academy  of  Dental  Surgery)  sujDpurative  inflammation  of  the 
gums  and  absorption  of  the  gums  and  alveolar  process. 

During  the  same  year  Scheff"^  of  Vienna  entitled  the  disorder 
periostitis  dentalis.  He  was  of  the  opinion  that  it  originated 
from  external  irritation  through  mechanical,  thermic  and  chemic 
changes.     The  real  origin  of  the  disorder  was,  in  his  opinion, 

'  Independent  Dental  Journal,  1875. 

''■  Philadelphia  Journal  of  Medical  and  Physical  Science,  1821. 

^  International  Dental  Journal,  Vol.  XIII. 

*  Journal  of  the  American  Medical  Association. 

^  Journal  of  the  American  Medical  Association. 

«  Dental  Cosmos,  Vol.  XXIY. 

'  Wiener  Med.  Presse,  Vol.  XVI. 


very  often  obseuve.  He  doubted,  liowever,  the  influence  of 
rheumatism. 

In  1876  Sirletti'(in  a  discussion  of  the  jmthology  of  the 
disorder,  which  he  called  alveolo-dental  periostitis)  regarded  it  as 
due  to  constitutional  conditions,  like  rheumatism,  scrofula,  syph- 
ilis, etc.,  with  local  causes  as  exciting  factors. 

In  1877  Rehwnikle,"  in  a  paper  on  pyorrhoea  alveolaris,  after 
citing  from  Albright  (of  Berlin)  the  claim  that  the  disorder 
was  due  to  uncleanliness,  mercury  and  the  suppression  of  habitual 
secretions,  expressed  the  opinion  that  acquired  and  inherited 
constitutional  defect  often  played  an  important  part  as  etiologic 
factors.  He  was  also  of  opinion  that  mercury  exerted  an  influ- 
ence in  its  causation.  Salivary  deposits  were,  in  his  opinion, 
without  influence.  Clowes''  was  of  opinion  in  1879  that  the 
general  cause  was  lack  of  nutrition  in  the  parts.  The  use  of 
wedges  often  excited  the  disorder. 

C.  J.  Essig,""  in  1880,  expressed  the  opinion  that  its  predis- 
posing causes  were  unknown,  that  it  occurred  as  a  rule  in  healthy 
persons,  and  that  irregular  and  crowded  teeth  acted  as  an  exciting 
cause. 

In  another  paper  during  the  same  year  G.  A.  Mills''' expressed 
the  ojiinion  that  the  disorder  was  of  systemic  origin.  Various 
mental  and  physical  influences  aided  its  progress,  such  as  nervous 
exhaustion  and  bodily  and  mental  overwork.  In  his  opinion  it 
frequently  occurred  in  children  and  adolescents  from  eruptive 
fevers.  The  deposit  was  only  a  local  manifestation  of  the 
disorder. 

In  1881  N.  S.  Niles'^  expressed  the  opinion  that  constitutional 
conditions  were,  as  a  rule,  without  influence,  and  that  local  irrita- 
ting deposits  w^ere  the  cause  in  twenty-five  j^er  cent  of  the  cases 
coming  under  his  observation.  He  was  of  opinion  also  that  the 
amount  of  lime  salts  taken  into  the  system  in  drinking  water 
exerted  an  influence.  A  calcic  and  j^hosphatic  diathesis  had  an 
influence  in  the  production  of  the  disorder. 

'  Gazzetta  Medica  di  Roma,  1S76. 

-Dental  Cosmos,  Vol.  XIX. 

■'  Ibid.,  Vol.  XXI. 

*  Dental  Cosmos,  Vol.  XXI. 

5  Ibid.,  Vol.  XXIII. 

"Ibid.,  Vol.  XXIV. 


4  IXTEESTITIAL    GINGIVITIS. 

In  1881  (when  there  seemed  to  have  been  many  contributions 
to  the  literature  of  the  subject)  Atkinson  ^  exjjressed  the  opinion 
that  nervous  debility  or  original  defect  in  innervation  exerted  an 
influence  in  the  production  of  the  disorder.  The  deposits  of 
tartar  were  a  secondary  consequence.  In  the  course  of  his  paper 
he  cited  the  opinion  of  Hamilton  Cartwright  that  Riggs's  disease 
commenced  in  an  unhealthy  condition  of  the  gums  with  a  sec- 
ondary deposit  of  tartar. 

In  a  paper  read  before  the  Dental  Section  of  the  Inter- 
national Medical  Congress,  Walker"  claimed  that  the  starting- 
point  of  the  disease  was  subacute  inflammation  passing  into  the 
depths  of  the  alveolar  process  adjacent  to  the  inflamed  gum.  In 
the  discussion  of  this  ^^ajjer,  Archovy  and  Joseph  Izklai,  of 
Buda  Pesth,  ascribed  the  disorder  to  minute  organisms.  Oakley 
Coles  thought  that  systemic  states  were  the  predisjDosing  factors, 
while  minute  organisms  exerted  an  exciting  influence. 

In  1882,  L.  C.  Ingersol  ^  regarded  sanguinary  calculus  as  a 
manifestation  of  the  disorder,  and  distinguished  it  from  salivary 
deposits. 

Malasses  and  Gallippe/  in  1884,  expressed  the  opinion  that 
the  disorder  was  of  microbic  origin. 

In  1885,  A.  O.  IlaAvls'^  expressed  the  opinion  that  the  causes 
were  environment  with  morbid  factors,  such  as  malaria,  excessive 
sodium,  etc.,  chloride  and  mercury. 

In  1886,  Reese**  expressed  the  oj^inion  that  the  disorder  had 
its  source  in  the  uric  acid  diathesis  resultant  on  abuse  of 
alcohol. 

During  the  same  year,  J.  D.  Patterson '  expressed  the  opinion 
that  the  disorder  was  of  catarrhal  origin.  Later,  in  1886,  J.  N. 
Farrar  ^  regarded  the  disorder  as  a  combined  result  of  systemic 
tendencies  and  local  irritants.  There  was  a  joeculiar  condition  of 
the  system  associated  with  hypersecretion  laden  with  increased 
earthy  deposits. 

'  Dental  Cosmos,  Vol.  XXIV. 

-  Transactions  of  the  International  Jledical  Congress,  1881. 

■'  Dental  Cosmos,  Vol.  XXV. 

*  Ibid.,  Vol.  XXVI. 

■-  Ibid.,  Vol.  XXVII. 

^Independent  Practitioner,  Vol.  VI. 

'  Dental  Cosmos,  Vol.  XXI. 

'*  Independent  Practitioner,  Vol.  VII. 


A.  R.  Starr  later  also  expressed  the  same  opinion.  He,  how- 
ever, was  unable  to  determine  the  local  irritation  factor,  but 
regarded  it  as  the  same  as  that  which  causes  exostosis  of  the 
cementum.     He  had  found  most  eases  in  the  upper  jaws. 

Black  ^  designated  the  disorder  phagadenic  pericementitis.  It 
was  a  specific  infection  of  an  inflammatory  character,  having  its 
origin  in  the  gingiva,  and  was  accompanied  with  destruction  of 
the  i^eridental  membrane  and  alveolar  walls. 

E.  S.  Talbot-  during  the  same  year  regarded  the  disorder  as 
a  local  one,  due  to  both  local  and  constitutional  causes.  The 
disorder  began  with  simple  inflammation  of  the  gums,  which 
afterward  became  chronic. 

Of  the  status  of  this  disease  at  the  close  of  the  year  liScSJ, 
the  following  analytic  picture  was  drawn  by  W.  X.  Sudduth^ : 
Pyorrhoea  alveolaris  is  a  term  ajjplied  to  the  secondary  stages  of 
a  disease  that  has  its  inception  in  a  catarrhal  stomatitis.  Being 
confined,  as  a  rule,  to  the  margin  of  the  gums  surrounding  the 
teeth,  it  might  be  called  a  "gingivitis,"  were  it  not  for  the  gen- 
eral catarrhal  tendency  shown  by  the  entire  mucous  membrane 
of  the  mouth  and  nasal  passages.  The  intimate  relation  between 
a  general  catarrhal  idiosyncrasy  and  pyorrhea  alveolaris  is  more 
than  mere  coincidence.  Its  common  occurrence  in  persons  who 
have  irregular  teeth  has  also  been  often  noted  by  Dr.  Budduth, 
who  considers  that  this  fact  has,  besides  the  matter  of  uncleanli- 
ness,  a  direct  bearing  upon  its  pathogeny.  It  is  well  known  that 
the  irregularities  of  the  teeth  present  an  indication  of  a  degener- 
ative taint,  and  that  jDcrsons  in  whom  irregularities  occur  are 
very  prone  to  catarrhal  affections  of  the  resiiiratory  organs, 
including  the  nasal  j)assage.  Their  skin  is  usually  very  suscep- 
tible to  inflammatory  affections.  Another  feature  is  offensive 
odor  of  the  saliva  of  individuals  who  show  this  particular  ten- 
dency to  catarrhal  affections  even  in  j)ersons  who  take  most  scru- 
pulous care  of  the  teeth.  In  the  majority  of  cases,  pyorrhoea  is 
a  stomatitis  in  which  the  local  and  constitutional  factors  in  tlie 
production  of  the  disease  are  largely  dependent  uj)ou  hereditary 
catarrhal  dyscrasia  for  their  ability  to  engraft  themselves  ujion 


American  System  of  ]  •entistry. 
•  Dental  Cosmos,  Vol.  XXVIII. 
'  Sajous'  Annual,  1888,  Vol.  Ill,  page  305. 


6  INTERSTITIAL    GINGIVITIS. 

the  tissues.  This  jjositiou  is  borne  out  by  the  clinical  experience 
of  Patterson,  of  Kansas  City,  Missouri,  who  reports  thirty-eight 
cases  of  well  marked  pyorrhoea  observed  by  him,  thirty-three  of 
which  presented  undoubted  evidence  of  nasal  catarrhal  condi- 
tions ;  two  were  the  result  of  direct  irritation  of  misfitting  partial 
plates,  and  the  remaining  three  were  apparently  caused  by  cal- 
cific deposits.  Patterson  remarks  that  a  close  examination  of  the 
history  of  the  above  quoted  cases  confirms  the  opinion  that  the 
disease  is,  as  a  rule,  an  "  oral  catarrh." 

From  the  foregoing  W.  X.  Sudduth  feels  justified  in  class- 
ing the  disease  as  a  localized  catarrhal  stomatitis  which  may  be 
either  acute  or  chronic.  Acute  catarrhal  inflammation  of  the 
gums  begins  in  circumscribed  points  which  present  a  bright  or 
rose-red  color,  and  which  are  generally  located  on  the  margin  or 
the  rugge  of  the  palate.  There  is  but  little  swelling  because  of 
the  dense  nature  of  the  sub-epithelial  connective  tissues.  The 
gums  present  the  same  stages  as  are  found  in  inflammation  of 
other  mucous  surfaces  —  first  dryness,  followed  by  an  increased 
secretion  of  mucus.  The  parts  are  very  sensitive  to  pressure ; 
the  patient  complains  pf  an  annoying,  burning  sensation.  The 
appearance  of  the  gums  is  noticeably  smooth  and  glistening. 
They  bleed  easily  when  the  brush  is  used  or  even  during  a  meal. 
This  stage  does  not  last  very  long,  but  soon  heals  by  resolution 
or  passes  into  a  chronic  catarrhal  stomatitis  in  which  condition 
the  gums  become  markedly  swollen  and  turgid.  They  present  a 
condition  of  tumefaction  that  sometimes  rapidly  jjasses  into 
hyj^ertrophy ;  at  other  times  there  is  an  indurated  appearance 
that  may  last  for  some  time.  Granulation  tissue  may  be  pro- 
duced as  the  result  of  overstimulation.  The  gums  become 
detached  from  the  necks  of  the  teeth ;  and  pockets  are  formed 
from  which  a  fetid  discharge  may  be  pressed,  giving  a  peculiarly 
disagreeable  odor.  Bullte  are  apt  to  form,  which,  by  rupturing 
in  the  process  of  mastication,  give  rise  to  intense  smarting.  The 
tongue  constantly  seeks  the  surface  if  it  be  on  the  inner  side. 

The  pathologic  changes  which  take  place  are,  according  to 
Newland  Pedley,  of  England,  "  hyj)ertrophy  of  the  muco-peri- 
osteal  fold  around  the  teeth,  accompanied  by  dilatation  of  capil- 
lary loops,  enlargement  of  the  papillae  and  rapid  proliferation  of 
ejiithelial  cells.    Later  the  gums  become  firm  and  contracted  and 


display  increase  of  fibrous  tissue.  The  cliauges  which  go  on  in 
the  socket  have  not  been  as  yet  satisfactorily  worked  out.  The 
examination  of  the  jaws  of  carnivora,  apparently  affected  with 
^jyorrhcea  alveolaris,  leads  to  the  suj)position  that  osteitis  of  the 
alveolar  process  spreading  toward  the  apex  of  the  socket  is  pres- 
ent. Later  the  alveolar  walls  become  absorbed  and  are  at  times 
more  or  less  denuded,  while  the  fangs  of  the  teeth  become  coated 
with  a  layer  of  thin,  hard,  green-lirown  tartar.  Ultimately  the 
disease  progressing,  the  teeth,  one  after  another,  drop  out." 

From  what  has  been  said  it  will  be  seen  that  the  pathology 
of  pyorrhoea  alveolaris  may  be  exj^lained  in  several  ways.  The 
general  causes  are  local  or  symptomatic,  or  both  combined.  The 
most  common  cause  of  catarrhal  gingivitis  is  found  in  local 
irritation,  combined  with  some  hereditary  disj)Osition  to  catarrhal 
affections.  The  next  greatest  etiologic  factor  is  symptomatic  — 
the  local  manifestation  of  a  constitutional  vice.  The  most  com- 
mon manifestation  is  that  of  syphilis  and  of  its  antidotes,  mercury 
and  potassium  iodide,  both  of  which  sometimes  find  expression  in 
a  localized  inflammation  which  may  be  the  starting  point  for 
jjyorrhosa  alveolaris.  As  a  complication,  of  the  disease  in  its 
secondary  stages  there  can  be  no  doubt  of  the  action  of  micro- 
organisms, but  Sudduth  does  not  feel  justified  in  conceding  to 
them  a  position  of  specificity. 

His  position  above  quoted  is  sustained  l3y  Pedley,  who  finds 
that  in  most  instances  it  is  due  to  some  constitutional  condition. 
The  fact  that  it  is  often  symmetrical  and  frequently  hereditary 
gives  support  as  to  this  view.  It  occurs  in  mouths  of  jjatients 
whose  health  has  been  undermined  by  debilitating  influences  and 
injudicious  habits  of  living.  It  is  a  common  sequel  of  malarial 
fever.  Young  persons  recovering  from  eruptive  fevers  are  some- 
times subjects  of  pyorrhoea  alveolaris.  Frequent  pregnancies  are 
a  fruitful  source  of  the  disorder.  Attention  has  been  lately 
drawn  to  the  shedding  of  the  teeth  in  tabes  dorsalis,  but  it  does 
not,  however,  seem  to  be  a  constant  symptom.  Pedley's  view, 
although  tending  entirely  toward  the  constitutional  character  of 
the  disease,  does  not  militate  against  its  catarrhal  nature. 

Bland  Sutton  has  found  shedding  of  teeth  frequent  in  rheu- 
matoid arthritis  in  animals.  He  has  also  met  with  it  in  mollities 
ossium    and  other  wasting  diseases.      Magitot    (who   views    the 


INTERSTITIAL    GINGIYITIS. 


alveolar  dental  periosteum  as  a  ligament  and  not  of  the  same 
nature  as  osseous  periosteum)  calls  the  disease  symptomatic 
alveolar-arthritis,  and  mentions  especially  as  causes,  chronic 
Bright's  disease  and  glycosuria,  in  which  latter  condition  the 
jjhenomenon  is  absolutely  constant. 

Patterson  holds  that  "  mouth-breathing  has,  in  his  expe- 
rience, been  a  very  common  accompanying  condition  which  he 
cannot  help  connecting  with  the  production  of  the  disease.  By 
it  the  gums  are  kept  dry,  their  functions  destroyed  and  the  way 
paved  for  catarrhal  inflammation.  The  majority  of  the  patients 
he  has  been  called  upon  to  treat  have  been  otherwise  healthy, 
robust  persons.  From  this  fact  he  does  not  favor  the  idea  of  the 
disease  being  dependent  upon  constitutional  derangement.  It 
is,  however,  a  well-known  fact  that  these  are  the  very  class  of 
people  who  when  irritation  is  once  set  uja  in  their  system,  present 
the  most  aggravated  cases,  by  reason  of  their  superfluous  vitality. 
He  says  he  has  occasionally  met  with  cases  where  the  local  con- 
dition was  evidently  aggravated  by  constitutional  derangement 
and  cure  was  thereby  retarded.  The  great  majority  of  eases, 
however,  have  shown  no  indication  of  constitutional  predisj)0si- 
tion,  but  have  j)ointed  unerringly  to  local  irritation  by  means  of 
which  the  function  of  the  mucous  membrane  had  been  destroyed." 

Syphilis  and  other  affections  may  engraft  themselves  upon 
the  gums  without  a  predisposition  of  the  parts  toward  an  inflam- 
matory condition,  and  having  disturbed  the  normal  status  of  the 
gingival  margins  they  pave  the  way  for  subsequent  disease  in 
the  alveolus.  Certain  drugs,  such  as  mercury,  phosphorus,  lead, 
etc.,  have  a  known  deleterious  action  upon  the  ligamentous 
attachment  of  the  teeth. 

In  1890  Miller  ^  expressed  the  opinion  that  the  disorder  was 
of  a  parasitic  nature. 

In  1892  C.  N.  Pierce"  charged  the  disorder  chiefly  to  sys- 
temic predisposition  and  enthusiastically  advocated  the  theory  of 
Reese  as  to  the  influence  of  the  uric  acid  diathesis.  In  1894 
W.  X.  Sudduth  ^  strongly  urged  the  influence  of  lactic  acid  as  a 
local  factor  in  the  disorder. 


'  Mioro-Organisms  of  the  Human  Mouth. 
-International  Dental  Journal,  Vol.  XIII. 
'Ibid.,  Vol.  XIV. 


HISTORY.  9 

John  Fitzgerald/  in  1899,  claimed  that  "  The  prodnction  of 
pyorrhoea  depends  upon  two  factors,  a  j^redisposing  cause  and 
•a  local  irritation.  The  predisposing  cause  may  be  tubercle, 
syphilis,  scurvy,  the  exhaustion  of  acute  infectious  diseases  or 
any  other  source  of  malnutrition.  The  exciting  cause  may  be, 
and  most  usually  is,  a  gingivitis  produced  in  one  of  the  ways  to 
be  presently  described.  There  is  also  a  pyorrhoea  of  gouty 
origin,  in  which  the  local  necrosis  of  the  peridental  membrane  is 
caused  by  gouty  disease  of  one  of  the  blood  vessels  in  its  sub- 
stance." 

The  views  on  etiology  of  this  condition  have  varied,  it  will 
be  observed,  from  purely  constitutional  causes  to  purely  local 
causes,  inclusive  of  microbic  affections.  In  the  main  it  will 
be  obvious,  however,  that  both  constitutional  causes,  whether 
inherited  or  acquired,  have  been  regarded  as  of  influence  by  the 
majority  of  those  who  have  written  on  the  subject.  There  has, 
however,  been  very  little  exact  stutly  of  either  the  predisposing 
or  the  exciting  causes  of  the  condition.  Even  the  impetus  given 
the  study  of  etiology  by  bacteriology  and  embryology  has  as  yet 
failed  to  make  itself  felt  to  any  considerable  degree  in  this 
department  of  dental  pathology. 

'  Clinical  Journal,  March  1, 1899. 


CHAPTER    II. 

INTRODUCTION. 

The  attempt  has  been  made  in  the  2>reseiit  work  to  reduce  to 
order  the  chaotic  notions  as  to  etiology,  pathology  and  treatment 
which,  during  the  present  century,  have  gathered  around  the 
morbid  condition  erroneously  entitled  Pyorrhoea  Alveolaris. 
AVhile  even  erroneous  titles  may  have  their  meaning  so  fixed  by 
usage  that  any  danger  from  the  error  involved  in  the  title  may 
be  j)ractically  nil,  still  this  is  not  the  case  with  the  title  just 
cited.  It  suggests  erroneous  etiology,  since  pyorrhoea  implies 
that  there  must  always  be  a  flow  of  pus,  and  hence  that  the  dis- 
ease must  always  result  from  infection  with  pus  microbes.  It 
implies  erroneous  pathology  and  erroneous  treatment  for  the 
same  reason.  This  being  the  case,  such  a  title  is  so  dangerously 
misleading  as  to  compel  in  the  present  stage  of  dental  science  its 
complete  disuse.  With  a  view  of  clearing  up  this  question  at 
the  outset  by  the  use  of  a  proper  title,  I  have  adopted  as  a  desig- 
nation for  the  condition  hitherto  known  as  pyorrhoea  alveolaris, 
the  term  "Interstitial  Gingivitis."  To  this  designation  (as  to  all 
•  other  attempts  to  express  within  a  small  space  an  extended  path- 
ology, etiology,  prognosis,  and  clinical  aspects)  there  are  some 
objections.  The  term  interstitial  is  used  by  some  pathologists  in 
a  limited  obscure  sense.  By  the  mass  of  dental  pathologists, 
surgeons,  physicians,  and  by  medical  lexicographers,  the  term  is 
■emjiloyed  in  precisely  the  sense  in  which  it  is  used  in  the  present 
Avork.  The  English  surgeon  and  lexicographer  Quain  defines 
interstitial  as  follows  :  "  Interstitial  (inter,  between  ;  and  sto,  I 
stand);  relating  to  the  interstices  of  an  organ.  The  term  is 
applied  in  physiology  to  the  tissue  which  exists  between  the 
proper  elements  of  any  structure,  namely,  some  form  of  connect- 
ive tissue.  In  pathology  the  word  is  used  in  connection  with 
absorption  when  a  part  is  gradually  removed  without  any  obvious 


INTRODUCTION.  11 

breaking  off,  and  also  to  indicate  the  imjjlication  of  the  intersti- 
tial tissues  in  morbid  processes  or  their  infiltration  with  morbid 
l^roduets,  as  interstitial  pneumonia,  interstitial  hepatitis." 

The  Encycloi^tedic  Medical  Dictionary  of  the  American 
Foster,  states  that  interstitial  has  three  significations :  First,  it  is 
applied  to  a  condition  disseminated  through  the  substance  of  an 
organ  or  part,  and  to  an  inflammation  afiecting  the  connective 
tissue  of  an  organ ;  second,  it  is  also  apj)lied  to  that  form  of  ^ 
growth  which  consists  in  the  interposition  of  new  elements 
between  old  ones,  instead  of  in  addition  to  the  surfaces ;  third,  it 
is  ajjplied  to  ijathologic  processes  occui^ying  the  space  between 
the  essential  parts  of  an  organ  which  constitute  its  proper  tissue, 
and  is  then  employed  in  a  sense  opposed  to  that  of  parenchy- 
matous. 

A  glance  at  the  illustrations  demonstrates  the  validity  of  the 
application  of  the  term  interstitial  (in  the  sense  of  Quain,  Foster, 
and  the  other  lexicographers)  to  the  condition  erroneously  called 
jjyorrhoea  alveolaris. 

I  have  adopted  the  term  gingivitis  for  reasons  which  will  be 
obvious  at  the  first  glance.  The  philologic  objection  may  be 
made  that  in  it  Greek  and  Latin  are  yoked  together.  Practically 
this  is  no  objection,  since  German,  French,  as  well  as  English, 
medical  authorities  employ  such  terms  of  mixed  origin.  Indeed 
the  French  (Mailhol '  for  example)  apply  the  term  gingivitis  to 
the  very  condition  to  which  I  have  applied  it.  In  addition,  they 
add  to  it  the  specific  term  "  expulsive,"  to  designate  "  a  form  of 
recession  of  the  gums,  accompanied  by  alveolar  osteoperiostitis, 
and  the  gradual  ex23ulsion  of  the  tooth  from  its  socket."  Foster  - 
suggests  the  substitution  of  the  term  ulitis  as  more  j)hilologically 
correct.  The  term  gingivitis,  however,  has  crept  into  such  wide 
use,  that  it  would  be  futile  to  attempt  to  displace  it  for  merely 
philologic  reasons.  The  two  terms  I  have  emialoyed  convey  a 
fairly  correct  idea  of  the  j^athologic  process  involved,  and  do 
not  imply  erroneous  views  as  to  etiology,  ^^athology,  prognosis 
and  treatment. 

The  pathologic  conception  adopted  in  the  present  work  anent 
interstitial  gingivitis  is  tlint  the  discirder  is  a  local  inflammatory 

'  Odontalgie. 
-Foster,  op.  cit. 


12  IXTEESTITIAL    GINGIVITIS. 

coiidition  of  the  gums,  tending  to  accelerate  their  normal  ten- 
dency to  disappearance  at  certain  periods  of  stress,  or  involution, 
of  which  involution  the  changes  jsroduced  by  old  age  are  a  tyjoe. 
In  this  early  senility  of  the  gums,  for  such  it  may  be  termed, 
two  great  types  of  causes  play  a  part ;  the  exciting  and  the  pre- 
disposing causes.  The  exciting  causes  may  be  purely  local,  or 
may  be  local  expressions  of  constitutional  states.  Thus  it  will 
be  shown  that  the  influence  of  uric  acid  when  present  is  exerted 
as  a  local  irritant,  and  not  as  a  constitutional  factor  —  the  theory 
urged  so  stronglj^  by  Pierce,  whose  views  have  been  of  late  so 
advocated  by  Kirk.^  The  uric  acid  hypothesis,  once  very  domi- 
nant in  medicine,  is  now  losing  its  force.  The  trend  of  medical 
oj)inion  is  to  consider  it  one  of  the  danger  signals  of  auto-intoxi- 
cation which  assumes  prominence  because  of  its  tendency  to 
excite  local  irritation.  It  is  but  one  of  a  number  of  local 
expressions  of  constitutional  defect.  This  view  of  the  influence 
of  uric  acid  in  etiology  the  present  work  will  try  to  demonstrate. 
Prominent  among  etiologic  factors  which  have  to  be  reckoned 
with,  are  pathogenic  germs.  In  the  present  work  it  will  be 
shown  by  all  laws  of  bacteriology  (under  which  investigations 
must  be  conducted)  that  there  is  no  specific  germ  which  is  capa- 
ble of  jDroducing  the  disease  itself,  and  furthermore,  that  the 
pyorrhoea  stage  of  the  disease  is  merely  a  complication  due  to 
jjyogenic  germ  infection  of  the  already  diseased  gums.  The 
views  of  Galijjpe  as  to  a  S23ecific  organism  will  be  shown  to  have 
failed  of  sup]3ort  by  numerous  control  experiments  described  in 
the  present  work.  As  these  have  been  conducted  by  different 
experimenters  they  are  free  from  the  personal  elements  of  error 
which  vitiate  the  researches  of  Galippe,  who  violated  that  canon 
of  the  laws  of  Koch  which  compels  production  of  the  disease  by 
the  alleged  specific  germ.  One  jJi'edisposing  factor  will  be 
shown  in  the  j^resent  work  to  be  the  nature  of  the  structures 
affected.  This  in  pathology  is  called  local  predisjjosition.  The 
gums,  etc.,  will  be  shown  to  be  transitory  structures  in  them- 
selves predestined  (as  already  stated)  to  certain  changes  at  cer- 
tain ages.  By  the  influence  of  the  disease,  about  to  be  discussed, 
these  changes  occur  prematurely.  The  influence  of  the  toxic 
agents  (mercury,  potassium  iodide,  etc.)  will  be  shown  to  have 

'  International  Dental  Journal,  May,  1899. 


INTKODUCTIOJf.  13 

been  exerted  constitutionally  through  the  central  nervous  system, 
their  local  effects  being  a  secondary  consequence  of  this.  The 
same  will  be  shown  to  be  the  case  with  conditions  like  scurvy 
(where  the  constitutional  factor  is  most  prominent),  and  with  the 
great  neuroses  (paretic  dementia,  locomotor  ataxia,  etc.).  Here, 
as  in  the  toxic  conditions,  one  great  element  considered  is  the 
influence  of  the  constitutional  conditions  upon  the  nerves  gov- 
erning local  blood  supply  and  tissue  waste  and  repair.  These 
influences  are  significantly  illustrated  in  the  various  processes 
described  later  which  tear  down  and  build  up. 

The  influence  of  morbid  heredity  as  a  direct  factor  will  be 
shown  not  to  be  great.  The  influence,  however,  of  degeneracy 
€xj)ressing  itself  along  the  lines  of  least  resistance  will  appear 
as  an  ominously  important  factor.  Heredity  here,  as  elsewhere, 
is  a  Avarning  rather  than  a  destiny. 

The  influence  of  the  nervous  system  on  the  processes  of 
growth  and  repair,  which  is  called  its  trophic  function,  has  been 
shown  to  play  a  part  in  both  the  etiology  of  the  disease  and  in 
its  progress.  This  function  has  received  but  little  attention  from 
dentists,  albeit  its  influence  has  been  recognized  in  dental  path- 
ology in  connection  with  great  neuroses  like  paretic  dementia 
and  locomotor  ataxia,  in  which  guiii  disorders  occur,  followed  by 
loosening  of  the  teeth.  The  pathology  of  the  disease  has  been 
discussed  in  the  light  of  established  facts  of  general  pathology 
which  have  been  accepted  by  the  leading  dental  investigators, 
and  not  merely  from  a  hypothetic  standpoint.  The  disease  has 
been  regarded  as  a  local  exaggeration  of  certain  physiologic  pro- 
cesses, accompanied  by  diminution  of  the  intensity  of  others.  In 
the  study  of  this  j^hase  of  the  question,  the  latest  researches  of 
dental  jjathologists  as  well  as  original  observation  and  exjieriment 
have  been  employed. 

Among  the  many  questions  which  the  present  treatise  is 
believed  to  settle  (so  far  as  exjserimentation  can)  is  the  following  : 
The  question  of  the  influence  and  nature  of  its  etiology.  It  is 
shown  that  here,  as  elsewhere  in  l^iology,  the  etiology  of  morbid 
conditions  has  many  phases  ;  that  in  it  exciting  and  predisjiosing 
causes  have  alike  to  be  considered ;  that  while  causes  may  be 
constitutional  in  origin  they  very  often  exert  their  action  locally  ; 
that  the  disease  is  not  a  product  of  civilization  nor  a  product  of 


14  INTERSTITIAL    GINGIVITIS. 

any  one  etiologic  factor ;  that  there  is  no  ground  yet  adduced 
for  believing  the  disease  to  be  specifically  infectious  and  due  to  a 
germ  of  a  sj^ecific  nature ;  that  in  it  the  germ  infection  occurs 
as  a  consequence  of  existing  disease,  and  is  not  the  cause  of 
the  morbid  condition,  but  one  of  its  stages :  Pyorrhoea.  The 
experiments  made,  as  well  as  the  pathologic  and  clinical  data, 
have  been  obtained  from  many  observers,  so  that  as  many  control 
observations  should  be  had  as  were  necessary  to  eliminate  per- 
sonal elements  of  error  inevitable  upon  original  observation  and 
research.  In  the  pathology  no  statement  is  made  which  is  not 
demonstrated  by  corroboratory  data,  including  a  photograph  of 
the  condition.  The  treatment  has  been  based  upon  the  pathology 
and  etiology.  Its  central  idea  is  that  the  human  being  must  be 
regarded  as  something  more  than  his  mouth  and  teeth  ;  hence  the 
duty  of  the  dental  scientist  is,  like  that  of  all  medical  scientists, 
best  shown  in  a  prophylactic  direction. 

The  pathologic  material  for  the  study  of  interstitial  gingivitis 
in  man  is  obtained  with  such  difficulty  in  the  recent  state  as  to 
necessitate  research  upon  animals.  This  disease  was  noticeably 
present  among  the  carnivora,  casually  inspected  in  American 
and  EuroiJean  zoologic  gardens.  Cats  and  dogs  were  also  known 
to  be  liable  to  the  disease.  As  the  first  step  in  investigation,  two 
practitioners  of  comparative  medicine,  with  an  extensive  hospital 
practice  (Dr.  Charles  E.  Sayre  and  Dr.  Alsoj)  E.  Flower),  were 
consulted  as  to  the  frequency  of  this  disease  in  animals.  All 
animals  under  their  care  suffered  from  it  more  or  less,  but  eighty 
per  cent  of  dogs  over  eight  years  of  age  had  the  disease.  Nearly 
every  dog  in  the  hospital  under  their  care  was  so  affected.  These 
dogs  comprised  all  breeds,  from  spaniels  and  terriers  to  the  New- 
foundland, St.  Bernard  and  great  Dane.  On  examination, 
every  phase  of  interstitial  gingivitis  was  found  in  the  mouths 
of  these  dogs,  from  its  inception  to  the  loss  of  the  teeth.  The 
number  of  dogs  observed  was  twenty-seven.  The  roots  of  the 
teeth  of  some  were  covered  with  deposits  and  so  exposed  that  the 
teeth  could  be  removed  with  the  fingers.  Such  diseased  mouths 
are  rarely,  if  ever,  present  in  human  beings.  The  outer  plate  of 
bone  was  absorbed,  the  roots  entirely  exposed,  pus  was  oozing 
from  around  them  and  the  mucous  membrane  was  badly  inflamed. 

It  should  be  remembered  that  the  jaw  of  the  dog,  like  the  jaw 


INTRODUCTION. 


15 


of  man,  is  undergoing  considerable  variation.  Like  man,  the 
dog,  having  put  himself  under  new  social  conditions  (so  to 
speak),  is  varying  greatly  both  as  to  brain,  skull  and  jaw  from 
his  wolf-like  ancestor.  As  he  is  under  the  protection  of  man, 
the  struggle  for  existence  as  to  food  is  less  intense  than  in  the 


Fjg.  1. 

wild  state  and  consequently  there  is  less  occasion,  even  for  fight- 
ing purposes,  of  his  jaw's  and  teeth. 

Independently  of  conditions  of  this  type,  many  of  the  dogs 
suffered  from  constitutional  disorders.  Eight  had  skin  diseases 
which  in  the  dog  are  more  likely  to  produce  obvious  consti- 
tutional defects  than  in  man.  Some  were  old  and  blind.  Borne 
had  been  injured  and  were  under  treatment  for  wounds.     Some 


16  INTEESTITIAL    GIjVGIYITIS. 

were  suffering  from  rachitis,  nervous  diseases,  and  were  over- 
bred.  Others  were  constipated  or  had  germ  tyj)es  of  diarrhoea. 
One  had  kidney  inflammation  and  bronchitis  with  high  fever. 
In  short,  these  dogs,  being  house  dogs,  presented  most  of  the 
constitutional  diseases  to  which  man  is  liable. 

The  month  of  a  Scotch  terrier  is  shown  in  Fm,   1.      The 


molar  and  premolar  had  been  removed  with  the  fingers.  The 
cuspids  and  incisors  are  quite  loose.  There  are  large  deposits 
of  tartar.  The  gum  and  alveolar  process  have  been  absorbed 
nearly  one-half  the  length  of  the  roots  of  the  teeth.  In  Fig.  2 
is  seen  the  mouth  of  a  Boston  terrier  with  the  incisors  and  j^re- 
molars    removed.      There    is   extensive   pyorrhoea.      There    are 


rXTRODUC'TIOX. 


17 


•calcic  deposits  uj)Oii  the  cuspids  and  molars.  There  is  recession 
of  the  gums  and  alveolar  process.  In  Fig.  3  is  shown  the  mouth 
of  another  Boston  terrier.  In  it  one  premolar  in  the  upper  and 
one  on  the  lower  jaw  have  been  extracted.  There  is  extensive 
inflammation  of  the  gum  about  the  molar,  cuspid  and  incisor 
with  large  calcic  deposits  about  the  teeth.     In  Fig.  4  are  shown 


teeth  covered  with  calcic  deposit  the  entire  length  of  the  root. 
These  teeth  were  removed  by  the  fingers  from  the  mouths  of  tAvo 
dogs,  one  of  whom  was  later  obtained  for  scientific  study.  This 
was  all  the  material  to  be  obtained  from  the  hospital,  since  the 
dogs  were  pets  Avho  had  been  placed  under  treatment  l)y  their 
•owners. 
3 


18  INTERSTITIAL    GINGIVITIS. 

Througli  the  courtesy  of  Poundmaster  Hugh  Curran,  the 
necessary  material  was  obtained  from  the  Chicago  Dog  Pound. 
Here  from  four  hundred  to  a  thousand  dogs  are  killed  per  week 
during  June,  July  and  August  each  year.  jSTinety-five  jser  cent 
are  mongrel  curs  leading  a  street  life,  hence  neither  luxu- 
rious diet  nor  luxurious  care  can  be  charged  with  any  disease 
in  them.  They  have,  at  least,  plenty  of  outdoor  exercise  and 
fresh  air.  Many,  despite  this  reversion  to  the  life  of  their  wolf- 
like ancestors,  have  skin  diseases  and  are  deaf  and  blind  from 
old  age.  The  bodies  were  secured  after  death,  at  which  time 
examinations  of  the  mouths  were  made.  Five  per  cent  of  the 
dogs  entering  the  pound  are  of  good  breeds.  These,  if  not  called 
for  by  the  owners,  are  sold  for  a  moderate  price. 

The  dogs  selected  for  the  death  penalty  are  collected  in  a 
large  box  pen,  leading  out  of  which  is  a  door  through  which  they 


Fici.  4. 

j)ass  into  an  air-tight  box.  Commpnicating  with  this  box  is  a 
stove  in  which  suljihur  is  burned  with  charcoal.  The  fumes 
pass  into  the  box  and  death  is  almost  instantaneous  and 
painless.  After  they  remain  fifteen  minutes,  a  door  leading  to 
the  air  is  opened  and  the  bodies  are  carted  away.  It  was  at  this 
time  that  access  was  had  to  them.  The  mouths  were  then  exam- 
ined. Such  cases  as  were  of  interest  were  placed  on  one  side 
and  the  jaws  removed  from  the  bodies.  Inside  of  one-half  hour 
the  S23ecimens  were  in  a  solution  to  be  kejjt  until  desired  for  use. 
Jaws  (with  interstitial  gingivitis  in  all  stages  of  jDrogress,  from 
simple  inflammation  of  the  gums  to  the  most  extreme  cases  of 
exfoliation  of  the  teeth)  were  obtained  in  an  abundance  for 
future  studies.  It  is  not  an  easy  matter  to  ascertain  the  ages  of 
these  animals.  In  a  general  way,  it  was  found  that  inflammation 
of  the  gums,  especially  about  the  canine  teeth,  was  almost  always 
present  in  dogs  over  one  year.     About  twenty-five  per  cent  of 


INTRODUCTION.  19 

these  dogs  at  four  years  of  age  had  the  (hsease,  eighty  per  cent  at 
from  eight  to  ten  years,  ninety-five  Y>er  cent  over  twelve  years  of 
age.  Since  I  commenced  my  investigation  (four  years  ago),  I 
have  examined  quite  a  large  number  of  dogs  about  homes,  but 
have  never  found  a  dog  over  four  years  without  this  disease  to  a 
greater  or  less  extent.  Many  house  dogs  at  one  year  had  inflam- 
mation of  the  gums.  Dogs  for  infection  and  those  used  for  mer- 
eurialization  were  picked  up  in  the  streets. 

Most  of  the  dogs  exhibited  at  the  last  three  animal  dog  shows 
held  in  Chicago  were  young,  ranging  from  one  to  four  years  of 
age.  About  twenty-five  per  cent  would  range  four  years  to 
eight.  Three  years  ago,  on  a  casual  examination  of  their  mouths, 
interstitial  gingivitis  was  found  to  be  common.  Occasionally 
recession  of  the  gums  and  pyorrhoea  alveolaris  occurred.  During 
the  last  two  years,  on  more  careful  examination,  twenty-five  j)er 
cent  of  dogs  between  the  ages  of  one  and  four  were  found  to  have 
interstitial  gingivitis  and  seventy-five  per  cent  of  dogs  from  four 
to  eight  years  were  found  to  have  interstitial  gingivitis  with 
recession  of  the  gums  and  pyorrhoea  alveolaris.  In  the  study  of 
this  disease^  therefore,  dogs  are  excellent  substitutes,  since  for 
l^athologic  research  they  can  be  obtained  at  an}"-  stage  of  the 
disease. 


CHAPTER    III. 

TRANSITORY    STRUCTURES. 


THE    JAWS. 


Because  of  man's  advance  in  evolution  and  because  of  the 
local  degeneracies  thereon  resultant,  through  the  law  of  economy 
of  growth  whereby  one  structure  is  sacrificed  for  the  benefit  of 
the  organism  as  a  whole,  the  face,  jaws,  teeth,  gums,  alveolar 
process  and  j^eridental  membrane,  being  varial^le  structures,  are 
^predisposed  to  disease  in  their  very  order  of  evolution. 

The  jaws  are  growing  smaller  because  large  ones  are  not 
required.  The  structures  are  changing  their  shapes  to  adapt 
themselves  to  the  new  environment.  Thus  —  instead  of  broad 
large  jaws  with  low  vaults;  short,  broad  alveolar  jjrocesses  with 
plenty  of  blood  supply  and  vitality  to  resist  mastication ;  teeth 
short,  with  large  bell  crowns  to  give  j^lenty  of  room  between  the 
roots  for  considerable  thickness  of  the  alveolar  jDrocess  for  the 
nourishment  of  the  jjeridental  membrane  and  supj^ort  and  pro- 
tection of  the  gum  tissue  —  small  narrow  jaws  occur  with  appa- 
rently high  vaults ;  long,  slender  and  thin  alveolar  processes, 
which  are  not  used  in  mastication  with  sufficient  force  to  carry 
the  blood  for  the  nourishment  of  the  tissues.  The  teeth  are 
changing  their  shape,  causing  the  roots  to  come  closer  together, 
and  thus  lessening  the  area  of  the  alveolar  process. 

That  the  jaws  of  man  are  growing  smaller  is  easily  demon- 
strated by  the  following  procedure :  Drop  a  j^erpendicular  line 
from  the  supraorbital  ridge,  whereu2:)on  it  will  l^e  found  that 
the  jaws  of  the  jirimitive  races  protrude  beyond  the  line,  as  is 
the  case  with  many  j^eoples  of  Europe  and  Asia  today. 

Mummery,  on  examination  of  the  skulls  of  two  hundred 
Britons  and  Roman  soldiers  in  Hythe  Church,  Kent,  Eng- 
land, found  the  narrowest  width  2.12  inches,  the  highest  2.62, 
Avith  an  average  of  2.50.  The  width  of  jaws  of  402  British 
soldiers   today  is :    narrowest    1.88 ;    widest  2.63,  average  2.28. 


TRANSITORY    SiTRUCTURES.  21 

The  highest  Avidth  was  very  rare,  only  eight  measured  2.50. 
The  jaws  of  the  mound-buihlers  compared  with  the  existing  cliff- 
dwellers  show  similar  results,  the  average  width  is  about  2.50 
inches.  Measurements  of  normal  jaws  of  855  Italians  of  Cen- 
tral Italy  were:  narrowest  1.88,  widest  2.G3,  average  2.17. 
Measurements  of  normal  jaws  of  4,935  Americans  gave  the  fol- 
lowing results  :  narrowest  1.75,  Avidest  (only  one  case)  2.56,  aver- 
age 2.13.  While  in  the  highest  type  of  primitive  man,  the 
width  of  the  upper  jaw  from  the  outer  surfaces  of  the  first  per- 
manent molars  near  tl,ie  margin  of  the  gum  was  2.50  inches  in 
diameter,  the  jaws  of  peop)le  now^  living  in  the  same  locality  are 
from  0.25  to  0.33  of  an  inch  smaller.  The  antero-j)Osterior 
diameter  has  also  shortened  from  one-half  to  five-eighths  of  an 
inch. 

Standing  on  the  corner  of  Picadilly  Circus  and  Regent 
street,  London,  in  the  fall  of  1897,  I  examined  the  faces  of 
10,000  passers-by  and  found  that  eighty-three  per  cent  possessed 
jaws  inside  of  the  perpendicular  line.  Of  3,000  English  school 
children  under  ten  years  of  age  ninety-three  per  cent  possessed 
jaws  inside  of  the  perpendicular  line,  thus  showing  a  difference 
of  ten  per  cent  in  one  generation. 

The  negroes  were  formerly,  in  the  02)inion  of  anthro2:)ologists,, 
in  the  main  a  long-headed  dolichocephalic  race  with  protruding- 
jaws.  Of  the  Northern  negroes,  who  in  the  main  have  white 
blood,  very  few  have  long  heads.  The  same  is  true  of  the  rela- 
tions of  the  jaAvs.  The  protrusion  of  the  jaws  has  largely  dis- 
appeared. 

That  the  jaw  is  becoming  smaller  is  further  shown  by  the 
disappearance  of  the  third  molar,  or  the  irregularities  resultant 
on  its  eruption  because  of  want  of  room,  or  its  erujation  with 
pain  for  like  reason.  In  the  primitive  races  it  is  large  and 
well  developed. 

THE    ALVEOLAR    PROCESS. 

The  alveolar  j)rocesses  are  sititated  upon  the  superior  border 
of  the  inferior  maxilla  and  ujDon  the  inferior  border  of  the 
superior  inaxilla.  These  bones,  considered  a  part  of  the  maxillary 
bones  often  so  described  by  anatomists,  should,  however,  be  con- 
sidered as  practically  distinct  bones  —  their  structure,  functions- 


22  INTERSTITIAL    GINGIVITIS. 

and  embryology  differ  so  completely  from  the  structure  and 
functions  of  the  maxillary  bones.  The  superior  and  inferior 
maxillae  are  (unlike  the  alveolar  processes)  composed  of  hard, 
compact  bone  structure.  The  large,  powerful  muscles  attached 
to  them  indicate  that  powerful  woi'k  is  to  be  accomplished. 
When  fully  developed  they  retain  their  full  size  through  life. 
The  alveolar  processes  are  composed  of  soft,  spongy  bone  of  a 
cancelloid  structure.  As  early  as  the  eleventh  week  of  intra- 
uterine life,  calcification  of  the  deciduous  teeth  commences,  and 
by  the  twentieth  week  calcific  material  is  abundantly  deposited. 
Ossification  is  also  rapidly  j)rogressing  about  the  dental  follicles. 
At  birth,  the  sacs  are  nearly  or  quite  inclosed  in  their  soft,  bony 
crypts,  and  the  crowns  of  the  teeth  upon  their  outer  surface  are 
composed  of  enamel,  which  is  dense  and  hard.  The  embryologic 
phases  of  the  dental  shelf  elsewhere  cited  indicate  this  develop- 
ment. 

The  alveolar  process,  being  soft  and  spongy,  molds  itself 
about  the  sacs  containing  the  crowns  of  the  teeth  and  about  their 
roots  after  their  eruption,  regardless  of  their  jDOsition  in  the  jaw. 
While  the  alveolar  jDrocesses  have  grown  rapidly,  they  have  up 
to  this  time  developed  only  sufficiently  to  cover  and  protect  the 
follicles  while  calcification  jjroceeds.  When  the  crowns  have 
become  calcified  and  the  roots  have  begun  to  take  in  their  calcific 
material,  absorption  of  the  borders  of  the  jiroeesses  takes  j)lace  in 
the  order  of  the  eruj)tion  of  the  teeth.  When  the  teeth  have 
erupted,  the  alveolar  j^rocess  develops  downward  and  upward 
with  the  teeth  until  they  attain  the  depth  of  the  roots  of  the 
teeth,  which  extend  in  most  instances  into  the  maxillary  l^ones  in 
the  anterior  part  of  the  mouth  at  least,  and  the  upper  and  lower 
teeth  rest  at  a  point  in  harmony  with  the  rami.  The  depth  at 
which  they  penetrate  the  bone. differs  in  different  mouths.  This 
depends  upon  the  length  of  the  roots  and  the  alveolar  process. 
This  in  turn  de2Dends  upon  the  length  of  the  rami.  The  incisive 
fossa,  the  canine  eminence  and  the  canine  fossa  give  evidence  of 
this  externally.  These  sockets  are  lined  with  extensions  of  the 
process,  thus  making  its  upper  l)order  irregular.  The  crypts  of 
the  permanent  teeth  are  located  at  the  apices  of  the  roots  of  the 
temporary  teeth.  The  permanent  teeth  have  large  crowns  which 
touch  each  other,  forming  a  line  to  the  jwsterior  jjart  of  the  jaw. 


TRANSITORY    STRUCTUEES.  23 

These  teeth,  as  they  erupt,  entirely  absorb  the  alveolar  j^i'ocess 
which  surrounded  the  temporary  teeth,  and  as  the  new  set  comes 
into  place  a  new  j^i'ocess  is  Ijuilt  up  around  them  for  their  sup- 
port. The  permanent  teeth  require  a  deeper  alveolar  process  to 
sujjjjort  their  roots,  which  are  much  longer  than  those  of  the 
temporary  teeth.  Hence  the  difference  in  the  depth  of  the  vault 
of  the  first  and  second  sets  of  teeth. 

The  alveolar  process  of  each  superior  maxilla  includes  the 
tuberosity,  and  extends  as  far  forward  as  the  median  line  of  the 
bone,  where  it  articulates  with  the  process  upon  the  opposite  side. 
It  is  harrow  in  front,  and  gradually  enlarges  until  it  reaches  the 
tuberosity,  where  it  becomes  rounded. 

The  process  is  composed  of  two  j^lates  of  bones,  an  outer  and 
an  inner,  Avhich  are  united  at  intervals  by  sej)ta  of  cancellous 
tissue.  These  forni  the  alveoli  for  the  reception  of  the  roots  of 
the  teeth.  In  some  cases  the  buccal  and  labial  surfaces  of  the 
roots  of  healthy  teeth  extend  nearly  or  quite  through  the  outer 
bony  plate  and  are  covered  by  the  peridental  and  mucous  mem- 
branes only. 

This  plate  is  continuous  with  the  facial  and  zygomatic  surfaces 
of  the  maxillary  bone.  The  inner  plate  is  thicker  and  stronger 
than  the  outer,  and  is  fortified  by  the  palate  bones.  The  external 
jilate  is  irregular  upon  the  outer  surface,  prominent  over  the  roots 
of  the  teeth,  and  depressed  between  the  roots  or  interspaces. 

With  the  change  in  the  size  of  jaws  there  is  also  change  in 
the  shape  of  the  vault  and  alveolar  processes.  When  the  dental 
arches  are  large,  measuring  from  2.25  to  2.50  inches,  the  vaults 
are  low  and  the  alveolar  processes  are  short  and  thick,  not  only 
giving  stability  to  the  teeth,  but  also  plenty  of  nourishment. 
Now  that  the  dental  arches  are  growing  smaller,  with  an  average 
of  from  1.90  to  2.00  inches,  the  vaults  are  higher  in  proportion, 
the  alveolar  processes  long  and  thin.  This  renders  the  teeth  and 
jaws  more  suscej^tible  to  trophic  changes  and  hence  to  disease. 
The  alveolar  process  in  the  anterior  part  of  the  mouth,  in  which 
the  incisors  and  cuspids  are  situated,  is  much  thinner  than  in  the 
posterior  parts. 

The  sockets  for  the  incisors  and  cuspids  are  conical  and  nuicli 
larger  than  any  of  the  other  single  sockets.  The  alveolar  pro- 
cess is  longer  and  thinner  than  at  any  of  the  other  teeth.  The 
3 


24  INTERSTITIAL    GIXGIVITIS. 

sockets  for  the  bicusj^ids  are  flattened  upon  their  anterior  and 
posterior  surfaces,  and  near  the  apices  tliey  are  frequently  bifur- 
cated. The  sockets  of  the  molars  are  large  at  the  openings. 
About  the  middle  of  their  length,  however,  they  are  divided  into 
three  smaller  sockets  for  the  reception  of  the  roots.  In  the  case 
of  the  third  molar  the  number  of  sockets  ranges  from  one 
large  cavity  to  three  or  four  of  smaller  size.  When  disease 
attacks  the  tissues,  destruction  is,  therefore,  more  rapid  in  its 
progress  in  the  anterior  parts  of  the  mouth  than  in  the  posterior, 
where  the  processes  are  thicker  and  more  nourishment  is 
requ^ired. 

The  septa  are  very  thin  at  the  margin  and  gradually  increase 
in  width  to  the  middle  of  the  jaw,  where  they  become  thicker, 
and  are  finally  lost  in  the  substance  of  the  jaw.  Some  septa  are 
thicker  than  others,  and  where  two  teeth  are  widely  sepa- 
rated, the  width  of  the  septa  naturally  corresponds  to  the  space 
between  the  teeth. 

What  is  true  in  regard  to  a  change  in  the  size  of  the  jaws  is 
also  true  in  respect  to  the  shape  of  the  crowns  of  the  teeth. 
While  they  are  not  growing  smaller  in  proportion  to  the  size  of 
the  jaws,  they  are  changing  shapes.  Once  they  were  quite  well- 
shaped,  giving  considerable  space  between  the  roots  for  a  thick 
alveolar  process,  thus  rendering  support  to  the  peridental  and 
mucous  membranes,  now  the  shape  has  changed.  The  proximal 
surfaces  are  almost  straight,  lessening  the  width  and  thus  allow- 
ing only  for  a  thin  septum,  with  barely  sufficient  surface  to  sujiport 
the  tissues. 

The  sockets  are  lined  with  a  thin  j^late  of  compact,  bony  sub- 
stance, extending  from  the  outer  and  inner  plates  of  the  alveolar 
process  to  the  apex,  where  there  are  small  openings  for  the 
entrance  of  the  nerve  and  blood  vessels  for  the  nourishment  of 
the  teeth. 

The  bony  plate  has  upon  its  inner  surface  the  elastic  periden- 
tal membrane,  which  acts  as  a  cushion  for  the  teeth,  while  it  is 
surrounded  by  a  spongy  bone. 

The  teeth  are  held  firmly  in  their  alveolar  sockets  by  the  peri- 
dental membrane.  Teeth  with  one  conical  root,  and  those  with 
two  or  more  perpendicular  roots,  are  retained  in  position  by  an 
exact  adaptation  of  the  tissues.     Teeth  having  more  than  one 


TEANSITORY    STEUCTUEES. 


25 


root  and  those  bent  or  irregular,  receive  support  from  all  sides 
by  reason  of  their  irregularity.  Fig.  5  (a  section  of  the  jaw  of  a 
cat)  illustrates  the  relative  position  of  the  teeth,  peridental  mem- 
brane and  alveolar  process  to  each  other. 

After  the  removal  of  the  permanent  teeth  the  alveolar  process 
is  entirely  absorbed.  Fig.  6  shows  how  the  absorption  takes 
place.  The  teeth  have  all  been  removed  from  the  superior  max- 
illa and  the  alveolar  process  has  been  entirely  absorbed.     The 


Fig.  5. — Ground  Section  of  Jaw  and  Teeth  of  Cat.     (Andkews.) 

molars  on  the  lower  jaw  having  been  extracted,  absorption  of 
the  alveolar  jDrocess  has  resulted  in  marked  contrast  with  the 
anterior  alveolar  process,  which  remains  intact  and  holds  the  teeth 
firmly  in  place.  It  is,  hence,  evident  from  the  changes  which 
occur,  from  the  first  development  of  the  teeth  to  their  final 
extraction,  that  the  alveolar  process  exists  solely  to  protect  the 
teeth  in  their  crypts  during  development  and  after  eruption. 
After  the  temporary  teeth  are  in  place  the  alveolar  process 
remains  unchanged  (except  l\y  gradual  enlargement  in  harmony 
with  the  growth  of  the  maxillary  bones)  until  about  the  sixth 
year,  when  the  second  set  ap]Dears.     The  crowns  of  the  perma- 


26 


INTERSTITIAL    GINGIVITIS. 


nent  teeth  require  more  space  than  those  of  the  temj^orary  set ; 
and  the  alveolar  process  must  necessarily  enlarge  to  accom- 
modate them.  This  enlargement  of  the  alveolar  process  is 
caused  chiefly  by  foi'mation  of  the  crowns  of  the  permanent 
teeth  before  eruption,  and  to  a  limited  extent  only  by  growth  of 


the  maxillary  bones.  These  may  cease  develoj^ment  at  any 
period  of  the  life  of  the  individual,  or  continue  as  late  as  the 
thirty-sixth  year.  As  diameter  of  the  crowns  of  tlie  permanent 
teeth  form  a  larger  circle  than  that  of  the  maxillary  bones,  the 


alveolar  process  must  necessarily  increase  its  diameter  and  pre- 
sent large  spaces  between  the  roots  of  the  teeth  for  the  devel- 
oj)ment  of  the  alveolar  process. 

The  process  is  solely  for  retaining  the  teeth,  and  if  for  any 
reason  the  dental  follicles  should  not  be  present,  and  the  tooth 


TRANSITORY    STRUCTITRES.  27 

sliould  not  eruj^t,  or  if  it  should  be  extracted  early,  the  process 
would  not  be  developed  at  that  point.  In  my  collection  of 
models  are  cases  of  arrested  development  of  the  alveolar  process, 
caused  by  the  lack  of  bicuspid  and  lateral  incisor  germs,  and  by 
extraction  of  deciduous  and  permanent  teeth. 

If  one  or  more  teeth  were  not  to  antagonize,  the  alveolar 
process  would  extend  beyond  the  natural  border,  carrying  the 
teeth  with  it.  A  marked  illustration  of  this  is  seen  where  the 
molars  are  decayed  to  the  gum  and  the  roots  remain.  The  vas- 
cularity of  the  process  may  be  such  that  hypertrophy  results. 
Excessive  development  of  the  alveolar  process  is  frequently 
observed  by  every  practitioner  in  connection  with  the  anterior 
inferior  teeth.  When  the  articulation  is  normal,  occlusion  of 
these  teeth  never  takes  place.  Frequently  (especially  in  patients 
from  six  to  twelve  years  of  age)  these  teeth  extend  to  and 
occlude  with  the  mucous  membrane  of  the  hard  palate.  Such  a 
case  is  illustrated  in  Fig.  7.  This  model  is  taken  from  the  jaw 
of  a  jDerson  thirty-seven  years  of  age,  but  this  excessive  develop- 
ment took  place  between  the  ages  of  six  and  twelve  years,  since 
at  that  period  the  vascularity  of  the  tissues  is  more  vigorous,  and 
the  development  of  the  process  more  formative  than  at  any 
period  subsequent  to  the  development  of  the  first  permanent 
teeth. 

In  one  case  under  observation  the  incisors  and  cuspids,, 
together  with  their  alveolar  process,  are  situated  upon  the 
external  surface,  while  the  biscupids,  molars  and  their  alveolar 
process  are  located  upon  the  inner  border  of  the  jaw.  In 
another  case,  the  alveolar  process  failed  to  cover  the  roots  of  the 
biscuspids  and  molars  upon  the  outer  surface,  the  teeth  having 
forced  themselves  into  a  larger  circle  through  the  alveolar  process 
by  the  contact  of  the  crowns.  The  roots  in  this  case  can  easily 
be  outlined  by  the  finger  through  the  mucous  membrane,  the 
outer  plate  of  the  alveolar  process  barely,  if  at  all,  covering  them. 
Tomes  ^  illustrates  a  case  of  faulty  development  of  the  outer 
plate  of  the  alveolar  process,  exposing  the  crown  of  the  tem- 
porary teeth.  This  occurred  in  a  hydrocephalic.  I  have  a 
number  of  models  showing  the  anterior  alveolar  process  project- 
ing beyond  the  normal  position  through  the  forward  movement 

'  Dental  Surgei')',  page  44. 


28  INTERSTITIAL    GINGIVITIS. 

of  the  molars.  This  may  be  due  to  a  natural  movement  of  the 
molars  forward,  or  the  process  may  be  forced  forward  by  the 
improper  occlusion  of  the  jaws.  The  teeth  are  moved  from  one 
position  to  another  simjjly  by  the  force  consequent  upon  absorp- 
tion and  deposition  of  bone.  This  is  noticeable  in  the  sjDaces 
between  the  centrals,  when  the  alveolar  process  develops  to  a 
larger  circle  than  is  necessary  to  accommodate  the  teeth.  The 
alveolar  processes  are  influenced  in  one  direction  or  the  other  by 
the  pressure  of  articulation.  This  results  from  inharmonious 
development  of  the  jaws.  The  teeth  may  come  together  in  such 
a  manner  as  to  throw  the  alveolar  processes  either  to  the  right  or 
the  left,  thus  j)roducing  a  full,  round  arch  uj)on  one  side  of  the 
jaws,  and  a  perfectly  flat  or  straight  arch  upon  the  other.  Occa- 
sionally both  u^Jj^er  and  lower  alveolar  processes  are  carried  for- 
ward in  the  same  manner.  The  alveolar  process  upon  the  lower 
jaw  is  more  liable  to  be  found  upon  the  inner  border  of  the  jaw 
than  is  the  ujjper  alveolar  process,  as  the  inferior  maxilla  is 
larger  and  more  dense  than  the  superior,  and  when  the  teeth  are 
once  in  position  upon  the  lower  jaw  they  are  not  so  liable  to 
subsequent  change.  Owing  to  this  the  teeth  of  the  su^Jerior 
maxilla  do  not  form  so  great  a  circle.  This  causes  the  teeth 
upon  the  sides  of  the  jaw  to  conflict,  and  the  lower  teeth  and 
alveolar  j^rocesses  to  be  carried  in,  while  the  anterior  teeth  of  the 
lower  jaw  are  held  inside  of  the  superior  anterior  teeth,  thus  car- 
rying the  alveolar  processes  inward. 

The  teeth  are  continually  changing  their  positions  in  the 
mouth.  This  is  as  often  beneficial  as  it  is  detrimental.  That  the 
teeth  may  perform  their  full  function,  they  should  not  only 
remain  firmly  in  the  alveolar  j)rocess,  but  they  should  also  antag- 
onize properly.  The  teeth  may  be  compared  to  the  bricks  in  an 
arch.  Remove  a  brick  and  the  arch  falls  to  pieces.  It  is  fre- 
quently found  that  the  teeth  do  not  articulate  properly ;  by  a 
slight  movement,  or  by  cutting  away  the  grinding  surfaces,  a 
better  articulation  may  be  secured.  When  this  operation  is  per- 
formed, the  teeth  move  in  their  sockets  by  absorj^tion  and  depo- 
sition of  bone,  demonstrating  the  fact  that  the  process  changes  in 
.shape  and  substance.  Ziegier'  says  absence  of  functional  use  is 
a  frequent  cause  of  j^remature  lacunar  absorption  of  the  bone. 

'  A  Text-Book  of  Special  Pathological  Anatomj',  page  145. 


TRANSITORY    STRUCTURES. 


29 


This  form  of  atrophy  from  disuse  occurs  not  only  when  a  limb  or 
a  part  of  a  limb  is  deprived  of  its  normal  activity,  but  also  when 
portions  of  a  single  bone  cease  to  perform  their  function  of  sup- 
port, and  finally,  like  all  the  bones  of  the  body,  as  age  advances, 
normal  or  physiologic  absorption  takes  place,  while  the  teeth  are 
still  in  the  jaws.  Unlike  other  bones  of  the  body,  however,  the 
absorption  of  the  alveolus  progresses  to  a  greater  extent  because 
of  the  unstable  condition  of  the  structures. 

From  what  has  already  been  said  of  the  vascularity  of  the 
alveolar  process,  it  is  evident  that  hypertrophy  of  tlie  tissue  may 


V^,.^^J|;'i'^'i  -i^iiA'Msm 


Fig.  8. 

ensue  from  an  unbalanced  nervous  system  and  from  simple  irri- 
tation of  varying  degree.  The  irritation  consequent  upon  the 
eruption  of  the  teeth,  together  with  the  excessive  blood  supply, 
are  both  primal  causes  of  overbuilding  of  tissue,  i.  e.,  hyperplasia. 

The  ragged  roots  of  the  temporary  teeth,  produced  by  absorp- 
tion of  the  gases  from  the  putrescent  pulps,  and  the  pressure  of 
the  permanent  crowns  against  the  tissues,  produce  sufficient 
stimulation  to  excite  physiological  action.  Tissue-building  gener- 
ally is  seen  in  connection  with  all  the  teeth,  and  the  process 
becomes  unnaturally  thick,  the  teeth  frequently  are  carried  in 
one  direction  and  another  ;  cementosis  of  the  roots  of  the  teeth 
and  hypertroijhy  of  the  process  result. 

In  cases  of  hypertrophy  of  the  alveolar  process,  enlargement 
is  associated  with  the  inner  plate  of  the  alveolar  process.  In 
cases  coming  under  my  ol)servation  the  inner  plate  in  most  is  the 


30 


ESfTERSTITIAL    GINGIVITIS. 


part  of  the  alveolar  process  affected  (Fig.  8  case).  The  outer 
plate,  although  quite  irregular  from  the  arrangement  of  the  teeth, 
is  usually  normal  in  thickness.  This  disparity  in  the  two  plates 
of  the  alveolar  process  is  due  to  the  fact  that  the  inner  plate  of 
the  alveolar  process  possesses  a  large  blood  supply,  the  i^osterior 
or  descending  palatine  arteries  furnishing  the  ossific  material.  I 
have  observed  but  few  cases  where  hypertrophy  has  extended  to 
and  included  the  outer  plate.  When  the  outer  plate  becomes 
involved  the  alveolar  process  assumes  a  very  thick  condition. 
Occasionally  hyjjertrophy  will  affect  one  side  only  or  one  distinct 


Fig.  9. 

locality  (Fig.  9).  In  this  case  the  enlargement  is  upon  the  left 
side  and  extends  from  the  first  bicuspid  posterior  to  and  including 
the  maxillary  tuberosity.  Instead  of  the  force  being  directed 
inward,  as  is  generally  the  case,  the  process  is  forced  outward  and 
backward.  This  enlargement  occurred  previously  to  the  develop- 
ment of  the  second  and  third  molars.  The  alveolar  process 
extends  downward  and  occludes  with  the  teeth  upon  the  lower 
jaw,  thus  preventing  the  molars  from  erupting. 

Under  the  microscope,  two  systems  of  Haversian  canals  are 
seen  in  the  alveolar  process.     Kolliker'  describes  these  as  follows  : 

"The  Haversian  canals  are  of  two  kinds.  One  with  the 
regular  lamellae  system  surrounding  it,  and  the  other,  the  so-called 

'  Handbuch  der  Gewebelehre,  page  272. 


TRANSITORY    STRUCTURES.  81 

Volkmann's  cauals,  containing  the  perforating  vessels  from  Von 
Ebner,  which  have  no  surrounding  h^nlell3e,  but  simply  penetrate 
through  the  layers  of  bone.  Volkmann's  canals  are  present  in 
all  tubular  bones  in  old  and  young.  While  especially  present  in 
the  outer  basal  lamellae,  they  occur  also  in  the  interstitial  leaflets 
and  in  the  inner  chief  lamellae  as  well  as  in  the  periosteal  layers 
of  the  skull  bone.  Here  their  number  is  very  variable  (Fig.  10). 
They  run  partly  transversely  or  obliquely,  and  also  partly  longi- 
tudinally, through  the  lamellae.     jNIany  of  these  canals  open  in 


iViTA^C''/ 


■h^ 


rKXF'BSt^  '"^ 


r^ 


Fig.  10. — Section  of  Bone  Showing  Blood  Vessels  of  Von  Ebner. 

the  outer  or  inner  surfaces  of  the  substantia  (compact  substance), 
and  also  here  and  there  in  the  Haversian  canals,  and  form  alto- 
gether usually  a,  wide-meshed  irregular  network.  In  their  struc- 
ture they  are  sometimes  smooth  and  sometimes  furnished  with 
dilatations  and  angles  projecting  in  and  out  in  profile.  The 
widest  has  a  diameter  of  100  micrometers  or  more,  and  the 
narrowest  not  more  than  10  or  20  micrometers,  and  there  are  still 
narrower  ones  which  are  altogether  obliterated,  appearing  like 
rings  or  circular-formed  structures  without  any  lumen,  or  like 
those  far  from  rare  obliterated  true  Haversian  canals  first 
described  by  Tomes  and  de  Morgan.  The  contents  of  the 
Volkmann  canals  are  the  same  as  the  Haversian  canals." 

Fig.  10  is  a  cross  section  of  the  medulla  of  a  calcified  human 


32 


INTERSTITIAL    GINGIVITIS. 


liumeiTis  slightly  eularged.  The  outer  lamellse  contams  a  large 
number  of  Volkmann's  canals  running  longitudinally  and  trans- 
versely and  extending  through  the  outer  jjlate  of  bone  into  the 
periosteum.  Fig.  11,  the  cross  section  of  the  section  seen  in 
JFig.  10,  shows  these  canals  more  highly  magnified.  The  Haver- 
,sian  canals  are  large  round  spaces  (Fig.  12),  containing  a  single 
artery  and  vein.  The  fine  hair-like  spaces  running  from  these 
large  spaces  are  the  canaliculi.  The  dark  sj^ots  circulating  each 
Haversian  canal  are  the  lacunte.  The  canaliculi  run  from  one 
lacunae  to  another  or  into  a  Haversian  canal  or  they  anastomose 
with  each  other.  The  rings  of  bone  about  each  Haversian  canal 
.are  called  lamellae.     The  lacunae  seem  to  be  about  uniformly 


-Section  of  Bone  (Hichee  Macmficvtion)  Sh 
Von  Ebner. 


ivG  Blood  Vessels  of 


•distributed    throughout    the    bone.      The    spaces    between    the 
lacunae  and  canaliculi  are  filled  with  lime  salts. 

A  longitudinal  section  of  bone  (Fig.  13)  is  similar  in  appear- 
ance to  the  cross  section.  Instead  of  the  lacunae  being  arranged 
in  rows  around  the  Haversian  canals  they  are  parallel.  It  will 
be  noticed  that  the  Haversian  canals  run  in  different  directions 
and    communicate  with  each  other  at  certain   intervals.      The 


TRANSITOKY    STEUCTITEES. 


33 


foregoing  deseriptiou,  with  illustrations  from  Kolliker,  is  essen- 
tially that  of  the  minute  anatomy  of  the  alveolar  j^roeess. 

THE    PERIOSTEUM    AND    PERIDENTAL    MEMBRANE. 

The  periosteum  is  a  fibrous  tissue  covering  the  outer  surface 
of  the  alveolus.  The  peridental  membrane  is  composed  of 
similar  structures  covering  the  roots  of  the    teeth    and  lining 


Fig.  12. —  Transverse  Section  of  the  Diaphysis  of  the  Htmercs  Magnified  350 

Times. 
a,  Haversian  Canal.     Dark  spaces,  Lacunar.     Hair-like  spaces,  Canaliculi. 

the  inner  wall  of  the  alveolus.  They  are  both  derived  from 
the  mesoblastic  layer.  For  this  reason  there  can  be  very  little 
difference  in  the  character  of  the  structure  of  each,  except  so  far 
as  function  is  concerned.  The  periosteum  is  made  up  of  four 
different  kinds  of  fibers.  An  outer  layer  of  coarse,  white  fibrous 
tissue,  an  inner  layer  of  fine,  white  fibrous  tissue,  elastic  fibers, 
and  penetrating  fibers  (fibers  of  Sharpey). 

The  fibers  of  the  periosteum  are  coarser  than  those  of  the 
]ieridental  membrane.     The  coarser  fibers  run  parallel  with  the 


34  IXTEESTITIAL    GINGIVITIS. 

alveolar  process  (J)  over  the  border  and  extend  as  far  as  the- 
union  of  the  ej^ithelial  layer  (E)  and  the  periosteum  (H),  Fig. 
14.  ("The  dental  ligament,"  Black. ^)  The  finer  fibers  run  in 
all  directions  and  enter  the  alveolar  process  at  every  point.  If  a 
section  of  the  alveolar  process  treated  with  acids  or  a  section 
affected  by  halisteresis  or  osteomalacia  be  placed  under  the 
microscope,  the  fibers  are  seen  to  retain  the  original  shape  of 
the  bone. 

The    fibers    of    the    periosteum,    therefore,     are    continued 
throughout  the  process  from  the  periosteum    on    the    one    side 


Fig.  13. — Longitudinal  Section  of  Bone  Magnified  100  Times. 
a,  Haversian  Canals,     h,  Lacuna  seen  from  the  side,     c,  Canaliculi. 

to  the  jDeridental  membrane  on  the  other.  This  is  also  illus- 
trated in  the  mouths  of  persons,  where  (after  wearing  artificial 
dentures  for  a  short  time)  heat  produces  absori^tion  of  the  lime 
salts,  leaving  the  fibrous  tissues  intact. 

The  periosteum  is  abundantly  supplied  with  blood  vessels 
which  anastomose  with  each  other  and  enter  the  alveolar  process- 
at  the  Haversian  canals.     The  plexus  of  blood  vessels  is  much 

'  American  System  of  Dentistry,  page  663. 


Fig.  14  — Longitudinal  Section  of  Tooth,  Alveolar  PfiOfEss,  Peridental  Memhrane  and 
Periosteum.     Nokmal  Tissue.    Sheep. 
B,  Dentine.       C,   Cementum.        E,   Epithelial   Tissue.        G,    Submucons    Membrane. 
H,  Periosteum.     J,  Alveolar  Process.     K,  Capillaries.     L,  Haversian   Canals.     M,  Fibrous 
Tissue.       AA,  Point  of  union  of  epithelial  tissue  and  peridental  membrane. 


X  7a.    A.  A.  obj.    Zeiss.    Micro-photographs,  reduced  one-third. 

Fig.  15. — Ceoss  Section  of  Tooth,  Alveolae  Peocess,  Peridental  Membrane  and 
Periosteum.     Normal  Tis.sde.     Dog. 

B,    Dentine.        C,    Cementum.        D,   Pulp.        H,    Periosteum.        J,    Alveolar  Process^ 
K,  Capillaries.      M,  Fibrous  Tissue.      U,  Nerve  Tissue.      C  T,  Connective  Tissue. 


TRANSITORY    STRUCTURES.  37 

larger  projiortionately  in  connection  with  the  alveolar  process 
than  with  other  bones  of  the  body,  owing  to  its  transitory 
nature. 

The  peridental  membrane  commences  at  the  margin  of  the 
epithelium  at  the  neck  of  the  tooth  AA,  Fig.  14,  and  is  attached 
directly  to  the  cementum.  This  membrane  has  various  func- 
tions :  First,  it  fills  the  s^^ace  between  these  two  structures, 
forming  a  cushion  for  the  teeth  to  rest  upon  ;  second,  like  the 
alveolar  process,  it  is  present  only  when  the  teeth  are  present, 
and  therefore  develops  with  the  alveolar  process  when  the  first 
teeth  erupt,  it  is  entirely  lost  when  the  temjDorary  teeth  are  shed,. 
is  restored  with  the  eru23tion  of  the  second  set,  and  when  the  per- 
manent teeth  are  extracted  it  disappears  with  the  alveolar  process 
completely  ;  third,  it  furnishes  the  nourishment  for  the  teeth 
while  they  are  in  position  in  the  jaw,  and  holds  them  in  their 
sockets. 

The  fibrous  tissue,  in  its  earliest  stages  comj)rises  nearly  all 
or  quite  all  of  that  portion  of  the  jaw  which  eventually  becomes 
the  alveolar  process.  Calcification  begins  at  the  center  of  the 
jaws  and  gradually  closes  in  upon  the  fibrous  membrane  until  it 
becomes  the  thickness  of  a  sheet  of  j)aper.  In  young  persons 
the  membrane  is  much  thicker  than  in  old  age,  since,  as  age 
advances,  the  osteoblasts  on  the  one  hand  and  the  cementoblasts 
on  the  other  send  out  new  material  and  each  wall  closes  in  upon 
the  membrane,  which  becomes  very  thin  in  old  age  and  almost  lost. 

The  fibers  which  compose  this  membrane  extend  in  all  direc- 
tions ;  some  crosswise  ^penetrating  the  cementum,  on  the  one 
hand,  and  the  alveolar  process  on  the  other.  In  a  general  way, 
since  the  fibers  extend  through  the  alveolar  wall,  they  are  more 
closely  adherent  to  the  bone  than  to  the  cementum,  and  usually 
cling  to  the  latter  when  the  tooth  is  removed.  It  will  be  observed 
that  these  fibers  do  not  enter  the  alveolar  process  uniformly  as 
claimed  by  Gray'  and  Pierce",  like  tacks  or  nails  driven  regularly 
into  a  board  (the  "fibers  of  Sharpey  "  Fig.  14),  but  vary  as  to 
quantity  in  different  localities.  In  some  localities  they  jjenetrate 
in  large  quantities  and  almost  surround  a  piece  of  alveolar  pro- 
cess, while  a  few  fibers  penetrate  but  a  short  distance.     In  some 

'  Anatomy. 

-  American  System  of  Dentisti-y,  page  668. 


38  INTERSTITIAL    GIN^GIYITIS. 

places,  they  caii  be  traced  almost  through  the  alveolar  process. 
These  fibers  are  much  finer  in  man  (Fig.  15)  than  in  the  lower 
animals  (Fig.  14,  dog).  In  connection  with  the  fibers  Avliich  jaass 
into  the  alveolar  process  are  numerous  blood  vessels.  Others  run 
diagonally,  and  still  others  lengthwise,  all  making  up  a  tissue 
which  holds  the  tooth  in  position  in  the  jaw.  The  fibers  enter 
the  peridental  membrane  at  all  j^oints  of  the  process,  from  its 
margin  to  the  apex  of  the  roots.  The  elasticity  of  this  membrane 
is  so  great  that  in  correcting  irregularities  a  tooth  may  be  turned 
from  one-fourth  to  one-half  around  without  breaking  the  fibers. 
The  elasticity  is  greatest  in  youth.  As  age  advances,  the  mem- 
brane grows  thinner  and  thinner  until,  late  in  life,  there  is  almost 
a  bony  union  between  the  tooth  and  the  alveolar  process,  thus 
preventing  stretching  of  the  fibers.  At  the  upper  border,  under 
the  gum  tissue,  these  fibers  extend  over  the  edge  of  the  alveolar 
border  and  unite  with  the  fibers  of  the  periosteum  on  the  outer 
border  of  the  process,  forming  the  interstitial  tissue. 

If  absorption  of  the  inorganic  substance  of  the  alveolar  jjro- 
cess  occurs,  the  fibrous  tissue  retains  the  shape  of  the  process. 
The  same  results  when  inflammation  of  the  peridental  membrane 
takes  place  at  the  gum  margin  or  at  the  apex  of  the  root  of  the 
tooth.  What  was  once  alveolar  process  is  now  peridental  mem- 
brane or  fibrous  tissue. 

Two  kinds  of  structures  are  present  in  the  alveolar  j^rocess — 
a  dense,  compact,  hard  structure  (comjjosed  of  lime  salts),  and  a 
fibrous  tissue ;  either  alone  will  retain  the  shape  of  the  tissue. 

Blood  vessels  permeate  this  membrane  throughout  from  the 
gum  tissue  at  the  neck  of  the  tooth,  through  the  alveolar  walls 
to  the  end  of  the  roots.  They  are  most  abundant  in  youth. 
Capillary  blood  vessels  enter  the  Haversian  canals  through  the 
process  and  into  the  cementum.  Many  of  these  blood  vessels 
extend  the  entire  length  from  the  gum  margin  to  the  apex  in 
straight  lines  and  vice  versa.  In  many  of  the  illustrations,  the 
blood  vessels  will  be  seen  to  follow  the  line  of  the  alveolar  j)ro- 
cess  (Fig.  14).  A  great  supply  of  blood  vessels  penetrate  the 
membrane  through  the  alveolar  walls.  These  vessels  unite  and 
anastomose  with  the  arteries  which  traverse  lengthwise,  forming 
a  complicated  plexus  (Fig.  16).  According  to  some  writers  the 
vascular  sup^jly  of  the  peridental  membrane  is  situated  in  the 


X  75.    A.  A.  obj.    Zeiss.    Micro-pliotographs.  reduced  one-third. 

Fig.  16. — Cross  Sehiin  of  Tooth,  Alveolar  Process  and  Peridental  Memdi!ane. 
Injected  Blood  Vessels.     Normal.    Dog. 

B,  Dentine.    C,  Cfmentum.     I,  Peridental  Membrane.    J,  Alveolar  Process.    K,  Capillaries. 
L,  Haversian  Canals. 


X  To.    A.  A.  011.1.     Zeiss.    .Micro-photoifrapUs.  reduced  one-third. 

Fig.  17.— Cboss  Section  of  Tooth,  Alveol.\k  Process  and  Pehidextal  Membrane. 
Injected  Blood  Vessels.    Normal.    Dog. 

B,  Dentine.     C,  Cementum.     I,  Peridental  Membrane.     J,  Alveolar  Process.     K,  Capillaries. 
L,  Haversian  Canals. 


TRANSITORY    STRUCTURES.  41 

center  of  the  structure.  This  has  not  been  my  experience.  All 
of  my  slides,  as  well  as  those  here  presented,  show  the  blood 
vessels  to  be  situated  nearest  the  alveolar  process.  It  is  quite 
natural  that  this  should  be  so,  since  very  little  blood  is  required 
for  the  nourishment  of  the  cementum,  while  the  largest  amount 
is  requii-ed  to  supply  the  alveolar  process.  The  system  of  blood 
vessels  situated  in  the  peridental  membrane  and  showing  their 
relation  to  the  surrounding  tissue  is  well  shown  in  the  injected 
specimen  from  healthy  dogs  (Figs.  16  and  17).  Pus  pockets  and 
abscesses  are  hence  more  liable  to  form  near  and  in  the  alveolar 
process  than  near  the  tooth  structure.  When  infection  takes 
place,  the  products  of  inflammation  are  carried  through  the 
blood  vessels  and  the  foci  of  round  cell  inflammation  are  located 
near  or  in  the  alveolar  process  where  abscesses  form.  The  vessels 
seen  in  the  membrane  anastomose  very  freely  with  those  at  the 
gum  margin,  showing  the  membrane  to  be  well  nourished  in  all 
its  parts.  Should  one  part  become  involved  by  disease  the  other 
parts  are  overnourished  in  consequence. 

These  .blood  vessels  enter  the  alveolar  walls  with  the  fibrous 
tissue  through  the  Haversian  canals  and  these  in  turn  permeate 
the  entire  bone.  As  age  advances,  however,  the  bone  Ijecomes 
more  dense,  and  the  Haversian  canals  become  smaller  and  (under 
certain  conditions)  cease  to  exist.  When  disease  takes  place, 
either  at  the  gingivus  or  at  the  apex  of  the  root,  the  supply  of 
blood  being  thus  cut  off",  the  tissues  receive  sufficient  nourishment 
through  the  alveolar  wall.  Since  the  structures  are  in  a  transi- 
tory state,  being  destroyed  an(^  rejjaired  so  frequently,  it  is  evi- 
dent why  the  blood  supply  is  so  rich. 

CALCOSPHERITES. 

Small,  hard  bodies  are  frequently  found  in  the  peridental 
membrane.  These  are  sometimes  in  the  form  of  concentric  rings 
of  lime  salts  and  are  called  calcospherites.  They  are  not  always 
round,  but  may  be  of  any  shape  and  vary  as  well  in  size.  They 
bear  the  same  relation  to  the  peridental  membrane  that  pulp 
stones  do  to  the  dental  pulp.  Black '  says :  "  I  have  seen  more  of 
them  about  the  roots  of  the  molars  than  elsewhere,  but  have 
found    them   along    the   sides    of   the   roots   of    the    bicuspids.'" 


'  Periosteum  and  Peridental  Membrane,  Pase  94. 


42  INTEESTITIAL    GINGIVITIS. 

When  irritation  and  inflammation  take  j)lace  in  the  peridental 
membrane,  the  cementoblasts  build  up  cement  substance,  just  as 
the  osteoblasts  do  in  the  alveolar  process  and  the  odontoblasts  do 
in  the  pulp  chamber.  tSometimes  they  are  attached  to  the  root 
of  the  tooth,  Avhich  produces  what  is  called  exostosis  or  cenien- 
tosis.  They  may  remain  unattached,  floating  in  the  fibrous  tissue. 
These  are  very  common  in  connection  with  interstitial  gingivitis. 

GUMS    AND    MUCOUS    MEMBRANE. 

The  tooth,  according  to  Minot,'  is  a  j^apilla  which  projects 
into  the  epidermis,  and  ossifying  in  a  particular  way,  changes  into 
ivory  around  the  soft  core  or  pulp.  To  the  laajnlla  the  epidermis 
adds  a  layer  of  enamel.  The  tooth  proper  unites  with  a  small 
Y>\ate  of  dermal  bone  at  its  base.  By  a  modification  on  the  jaw, 
the  epidermis  first  grows  into  the  dermis,  and  then  the  dermal 
tooth  papilla  is  developed.  The  teeth  were  primitively  organs  of 
the  skin  and  widely  developed  over  the  surfaces  of  the  body.  As 
the  mucous  membrane  is  practicall}^  a  continuation  of  the  skin,  it, 
in  accordance  with  the  law  of  individuation,  became  specialized 
and  lost  some  of  the  functions  of  the  skin  while  developing  the 
others  to  greater  perfection. 

The  mucous  membrane  lines  the  cavity  of  the  mouth,  the 
nose,  and  extends  through  the  larynx  into  the  lungs  and  through 
the  oesophagus  into  the  stomach.  It  covers  the  tongue,  jaws, 
alveolar  process,  dipping  down  between  the  necks  of  the  teeth 
and  the  alveolar  process  as  far  as  the  peridental  membrane,  leav- 
ing a  free  space  between  the  membrane  and  the  teeth  through  its 
entire  length. 

It  consists  of  two  layers  (Fig.  18),  the  epithelium  (A)  and 
corium  (B),  sej^arated  by  the  basement  membrane  (C).  The 
epithelium  is  composed  of  the  epithelial  cells :  First,  one  row  of 
columnar  cells  (B)  situated  upon  the  basement  membrane  (C); 
second,  two  rows  of  six-sided  prickle  shells  (E);  third,  two  rows 
of  six-sided  cells  (F);  fourth,  two  or  three  rows  of  squamous 
cells  (G) ;  and  fifth,  four  or  five  rows  of  flattened  dead  cells  (H), 
which  were  originally  the  columnar  cells  upon  the  basement 
membrane.  The  young  new  cells  are  the  columnar  cells  which 
jaass  from  one  stage  to  another,  changing  their  shapes  until  they 

'  Embryology,  page  481. 


TRANSITORY    STRUCTURES. 


4a 


eventually  become  dead  cells  and  are  exfoliated  from  the  surface 
of  the  tissue.  The  basement  membrane  (C)  is  made  up  of  fillers 
running  longitudinally,  from  papillae,  which  allow  the  tunica 
propria  containing  blood  vessels  and  nerves  to  pass  up  into  the 
epithelium  structure. 

The  corium  (B)  (which  lies  below  the  basement  membi-ane) 
is  composed  of  alveolar  connective  tissue,  white  yellow  fibrous 
connective  tissue,  muscular  fibers,  nerves,  blood  vessels  and 
lymphatics.  It  is  made  up  of  the  tunica  propria  and  the 
submncosa. 


Fig.  is. — Diagrammatic  Illustkatio.v  of  the  Epithelium  and  Submucous  Laykus  ok   tiik 
Mucous  Membrane. 

A,  Epithelium.      B,  Coriuni.     C,  Basement  Membrane.     D,  Columna  Cells.     E,  Prickle 
Cells.     F,  Six-sided  Cells.    G,  Squamous  Cells.    PI,  Flattened  Dead  Cells. 

.  The  tunica  jDropria  (beautifully  shown  in  Fig.  19)  consists 
of  interlacing  connecting  fibers  interspersed  with  much  elastic 
fibrous  tissue.     This  tissue  penetrates  the  epithelial  layer  in  the 


44  INTERSTITIAL   GINGIVITIS. 

form  of  cone-sliaped  papillfe,  varying  in  length  with  the  thick- 
ness of  the  epithelium.  This  layer  being  the  thickest  at  the 
gum  margin  (E),  these  j^apillse  are  the  longest  and  largest  at  this 
locality.  The  fibers  of  the  tunica  propria  pass  gradually  into 
the  submucous  membrane  (G),  and  from  there  into  the  j^erios- 
teum  and  peridental  membrane  (M),  so  that  it  is  difficult  to 
determine  the  mucous  capacity  line  of  demarcation  separating  the 
different  structures.  The  submucosa  is  composed  of  fibrous 
connective  tissue  of  a  much  less  compact  variety.  This  structure 
is  attached  to  the  bones  through  the  j)eriosteum  and  peridental 
membrane.  In  this  structure  the  glands,  Ijlood  vessels,  nerves, 
fat  cells,  etc.,  occur. 

The  larger  blood  vessels  (K)  are  found  in  this  structure. 
From  these  large  blood  vessels  small  capillaries  extend  to  the 
tunica  propria.  It  is  here  that  infiammation  commences  in 
interstitial  gingivitis.  Numerous  veins  accom2)any  each  artery, 
and  lymphatics  form  a  network  around  them.  Small  nerve 
filaments  are  also  in  this  structure,  which  pass  through  the  tunica 
propria  and  into  each  j^apilla  in  connection  with  the  capillaries. 
The  terminal  nerve  fibers  come  in  contact  with  the  muscular 
fibers,  so  that  there  is  direct  communication  by  blood  vessel  and 
nerve  throughout  the  mucous  membrane  from  the  nose,  stomach 
and  lungs.  The  gum  tissue  is  very  thick  and  made  wp  of  fibrous 
tissue  running  in  three  or  four  directions,  rendering  it  dense, 
tough  and  hard.  The  membrane  thus  differs  from  the  same 
structure  in  other  parts  of  the  body.  On  account  of  these 
numerous  fibers,  this  structure  is  bound  tightly  to  the  alveolar 
process.  The  gum  tissue  acts  as  a  cushion  and  protection  from 
irritation  which  may  arise  from  hard  substances  being  taken  into 
the  mouth.  As  this  membrane  passes  and  coalesces  with  the 
membrane  of  the  lips  and  cheeks,  it  becomes  much  thinner  and 
less  dense.  In  the  center  of  the  tooth,  the  parallel  fibers  in  the 
tunica  propria  are  composed  of  flattened  fasciculi  of  connective 
tissue.  There  are  three  sets  of  fibers  —  those  which  run  verti- 
cally, those  which  radiate  and  are  fan-shaped,  and  those  which 
are  horizontal. 

The  mucous  membrane,  like  the  alveolar  process  and  peri- 
dental membrane,  is  comjDOsed  of  very  unstable  tissue.  It 
changes  its  structure,  blood  vessels  and   nerve  system  as  often 


X  75.    A.  A.  obj.     Zeiss.    Mici'O-pliotographs,  reduced  one-third. 

Fig.  19. — Longitudinal  Section  of  Tooth  and  Gum  Tissue.    Dog. 

D,  Dentine.  E,  Epithelial  Tissue.  G,  Submucous  Membrane.  K,  Capillaries.  M,  Fibrous 
Tis.'ue.  V,  Violent  Inflammation.  AA,  Point  of  Union  of  Epithelial  Tissue  and  Peridental 
Membrane.     RR,  Space  Pocket  from  '\^'a^t  of  Union  of  the  Epithelial  Fold. 


46  INTERSTITIAL    GINGIVITIS. 

as  the  other  structures.  Its  blood  vessels  and  nerve  system  are 
continually  renewing  connective  tissue,  periosteum  and  jaeridental 
membrane. 

A  difference  is  noticed  in  the  structui'e  of  the  papillary  layer 
in  man  and  the  lower  animals,  such  as  the  dog,  the  sheej)  and 
the  calf.  In  man  the  gum  tissue  is  not  so  thick,  therefore  the 
papillae  are  broader  and  shorter,  while  in  the  lower  animals  the 
paj^illfe  are  narrow,  long  and  more  closely  set  together.  Blood 
vessels  and  nerves  are  not  so  numerous  and  close  together  in  man 
as  in  animals. 

DO    GLANDS    EXIST    IN    THE    MUCOUS    AND    PERIDENTAL 
MEMBRANES  ? 

A  somewhat  widespread  ojiinion  locates  sj)ecial  glands  in  the 
gingival  tissues  and  the  peridental  membrane.  This  seems,  to  a 
certain  extent,  to  be  in  part  due  to  the  lack  of  definite  knowl- 
edge as  to  the  etiology  of  interstitial  gingivitis,  and  in  part  to  the 
fact  that  certain  constitutional  conditions,  such  as  mercurial  and 
potassium  iodide  poisoning  and  scurvy,  manifest  themselves  in 
the  gum  tissue  in  a  way  similarly  to  their  action  in  the  glandular 
structures  of  the  body.  Black  ^  claims,  for  example  :  "  That  part 
of  the  gingival  margin  that  lies  in  against  the  neck  of  the  tooth 
is  of  a  different  structure  from  its  other  parts.  Here  it  is  clothed 
with  a  very  soft,  round  or  polygonal  gland-like  epithelium  that 
suggests  the  formation  of  a  giand,  but  fails  to  assume  the 
glandular  structure,  though  it  seems  to  have  been  regarded  as 
such  by  Serres.  This  —  which  I  shall  call  the  gingival  organ  — 
emits  a  profusion  of  small  rounded  cells  Avhich  are  always  found 
in  the  saliva  (Salter)  and  are  usually  called  mucous-corj)uscles. 
It  is  well  known  that  certain  glands  have  the  power  of  the  selec- 
tion and  excretion  of  certain  j^oisons,  and  in  this  way  of  elimi- 
nating them  from  the  system,  and  that  if  the  substance  be  in 
large  amount,  hyjDersemia,  or  even  inflammation,  may  result.  It 
is  also  known  that  mercury  and  potassium  iodide  will  produce 
inflammation  of  the  free  margins  of  the  gums,  and  Salter  has 
found  that  these  cells  are  in  greater  abundance  under  these  cir- 
cumstances ;  also  that  the  cells  taken  from  the  o-ingival  border 


'  American  System  of  Dentistry,  pages  955-956. 


X  75.    A.  A.  obj.    Zeiss.    Micro-photographs,  reduced  one-third. 

Fig.  20. — Longitudinal  Section  of  Gum.     Nor.m.il  Tissue.     Sheep. 

C,  Cementum.  E,  Epithelial  Tissue.  G,  Submucous  Membrane.  K,  Capillaries. 
M,  Fibrous  Tissue.  A  A,  Point  of  Union  of  Epithelial  Tissue  and  Peridental  Membrane. 
Nm,  Naysmith's  Membrane.     Sg,  So-called  Glands  of  Serres. 


48  IJiTTEESTITIAL    GINGIVITIS. 

and  submitted  to  chemical  tests  after  the  person  has  taken  potas- 
sium iodide,  are  found  to  yield,  and  are  tinged  with,  iodin." 

Longitudinal  sections  of  the  tooth,  alveolus  and  surrounding 
tissues,  under  the  microscope,  exhibit  a  very  peculiar  formation 
of  the  mucous  membrane  at  its  line  of  union  with  the  peri- 
dental membrane  at  the  neck  of  the  tooth.  Black'  (in  an 
article  beautifully  illustrated  by  Frederick  Noyes)  seems  to 
identify  these  with  the  so-called  glands  of  Serres,  or  gingival 
glands  (Fig.  20).  He  speaks  of  them  as  glands  in  various 
places  throughout  the  article ;  for  example,  "  But  little  can  now 
be  said  of  the  function  of  the  network  of  glands  of  the  periden- 
tal membrane,  beyond  what  is  indicated  by  their  form,  location 
and  histological  characters.  With  the  knowledge  of  their  posi- 
tion and  general  character,  clinical  observation  leads  to  the  con- 
clusion that  they  are  readily  disturbed  by  certain  drugs,  notably 
by  mercury  and  iodin ;  and  that  they  are  often  disturbed  by 
.substances  poisonous  to  them  floating  in  the  blood  streams.  This 
is  evidenced  by  the  appearance  of  marginal  gingivitis,  with 
soreness  of  the  peridental  membrane.  Such  disturbances  would 
not  be  likely  to  occur  without  the  presence  of  some  specialized  or 
secretory  tissue.  ...  It  seems  to  me  very  certain  that  the 
disease  which  I  have  described  as  phagedenic  pericementitis  has 
its  seat  in  these  glands."  Black,  however,  does  not  seem  quite 
certain  of  the  validity  of  his  position,  since  he  further  remarks, 
""Though  definitely  lobulated,  this  l3ody  does  not  seem  to  possess 
the  characters  of  a  gland,  and  I  should  not  sup2')0se  from  an 
examination  of  its  tissues  that  it  had  a  glandular  function.  It 
encircles  but  a  portion  of  the  neck  of  the  tooth,  usually  only  the 
approximal  portion,  thinning  away  toward  the  buccal  and 
lingual,  so  that  in  many  of  the  lengthwise  sections  it  may  be 
very  small,  or  does  not  ajipear  at  all." 

In  many  slides  of  sections  from  canine  jaws  and  human,- the 
same  jDCculiar  arrangement  of  structure  was  observed,  although 
not  in  so  marked  a  degree.     In  the  immature  herbivora  (calf  and 


^  Dental  Cosmos,  February,  1S99. 

-  The  material  obtained  for  rnaking  slides  from  man,  other  tlian  the  scurvy  cases, 
■fl'as  obtained  through  the  kindness  of  surgeons  from  jaws  removed  from  hospital 
patients,  as  a  result  of  disease ;  the  surgeons  placing  them  into  alcohol  or  Miiller's 
solution  as  soon  as  removed. 


^t^XS^Tv 


w;- 


.V 


«;^ 


w 


D. 


\ 


X  75.    A.  A.  obj.    Zeiss.     Micro-photographs,  reduced  one-third. 

iFiG.  21.— Ceo.¥s  Section-  of  Tooth   and  Peridental  Membrane.      Norm.\l  Tissue.     Sheei'. 

C,  Cementurn.     D,  Dentine.     I,  Peridental  Membrane.    TV,  Epithelial  Debris. 


X  300.    No.  2  projection  ocular.     D.  D.  obj.    Zeiss.    Micro-photographs,  reduced  one-third. 

Fig.  22. — Cross  Section  of  Tooth  and  Peridental  Membkane.      Noemal  Tissue.      Siiebp.- 

C,  Cementum.     D,  Dentine.     I,  Peridental  Membrane.     W,  Epithelial  Debris. 


TRANSITOEY    STRUCTURES.  51 

lamb)  these  jieculiar  formations  of  structure  are  well  marked, 
albeit  less  so  in  the  carnivora,  and  still  less  in  man. 

Were  glands  present  in  this  locality  it  is  logical  to  infer  that 
they  would  become  involved  in  mercurialism,  plumbism  and 
scurvv,  and  exhibit  marked  inflammation  with  liroken-down 
structures  in  a  given  locality,  as  at  the  union  of  the  gum  tissue 
with  the  peridental  membrane.     Such  a  case  is  unknown. 

The  mucous  membrane  under  the  microscope  appears  at  a 
point  between  the  teeth  (and  faintly  so  at  the  inner  and  outer 
border  as  shown  by  Black)  to  double  upon  itself.  When  the 
tooth  erupts,  absorption  of  the  gums  occurs  at  the  highest  point. 
The  gum  tissue  passing  down  to  the  neck  of  the  tooth  folds  or 
crowds  upon  itself  between  the  teeth  with  a  peculiar  cur^-e 
downward,  inward  and  then  outward  and  upward.  At  the 
upper  border,  about  midway  from  the  gingival  margin  to  the 
neck  of  the  tooth,  may  be  seen  a  space  or  pocket  (never  twice 
alike  in  appearance)  where  the  edge  of  the  gum  tissue  comes  in 
contact  with  the  original  epithelium.  Sometimes  the  space  or 
2)0cket  is  closed  up  (Figs.  48,  44,  51).  Again  it  remains  open 
(Figs.  19,  32,  50,  53).  Frequently  this  peculiar  type  of 
structure  is  absent,  showing  that  the  fold  of  gum  tissue  either 
has  been  absorbed  in  the  eruption  of  the  tooth  or  did  not  form. 
This  peculiar  form  encircles  only  a  portion  of  the  neck  of  the 
tooth  (according  to  Black's  examination  of  the  structure  in 
sheep).  This  in  itself  seems  to  offset  the  glandular  theory,  since 
gingivitis  almost  invariably  starts  on  the  lingual  or  palatine  and 
labial  surfaces  where  this  structure  does  not  appear.  In  the 
slides  of  the  scurvy  case  there  does  not  aj^pear  the  slightest 
evidence  of  anything  resembling  glandular  structure.  Hence 
it  would  seem  safe  to  conclude  that  the  glandular  structure  does 
not  occur  in  this  locality.  It  is  by  no  means  impossible  that  in 
the  peculiar  epithelium  in  this  locality,  epithelial  cells  undergo 
changes  which  to  some  observers  simulate  glandular  structure, 
but  on  histologic  analysis  are  distinguishable  trom  it,  resemliling 
in  this  the  crypts  of  the  head  of  the  penis. 

In  cross  sections  of  the  peridental  membrane,  with  a  low 
2)ower  may  be  seen  dark  bodies  arranged  along  the  margin  of  the 
cementum  in  the  peridental  membrane  (Fig.  21).  They  are 
more  numerous,  however,  near  the  o-inoiyal  liorder  than  at  the 


52 


IN^TEESTITIAL    GINGIVITIS. 


root  extremity.  These  bodies  are  more  numerous  and  better 
defined  in  the  sheep  than  in  the  calf,  and  more  ajiparent  in  the 
canine  jaw  than  in  the  human.  Under  higher  power  (Fig.  22) 
they  may  be  distinctly  demarcated  as  epithelial  cells  arranged 


** 

'  -Sfc^ 

'  ^':' 

«*;  ■; 

ss»  \ 

ik 

«^ 

i 

j 

-■•"t 

IBI^ 

X  560.    No.  2  projector  ocular.    One-twelfth  obj.    Zeiss. 

Fig.  23. — Ceoss  Section  of  Tooth  and  Peridental  Membrane.     Normal  Tissue. 

Sheep. 

C,  Cementum.    D,  Dentine.    I,  Peridental  Membrane.    W,  Epithelial  Debris. 


in  single  rows  of"  loops,  again  in  double  rows,  again  in  rows  of 
three  and  sometimes  in  round  or  oblong  groups,  with  clusters  of 
cells  without  shape  or  form.  With  a  still  higher  magnifying 
power  (Fig.  23)  it  will  be  seen  that  these  masses  of  cells  are 
polygonous,  never  prismatic.     They  hence  are  similar  in  shape 


TRAXSITORY    STRUCTURES.  53- 

to  the  epithelial  cells  situated  above  the  columnar  cells.  They 
also  resemble  the  cells  which  are  situated  inside  of  the  epithelial 
lamina.  In  the  larger  amplification  the  nucleus  can  be  readily 
observed. 

Black '  has  attempted  to  demonstrate  that  glands  exist  in 
the  structure  and  that  the  cells  last  mentioned  are  glands. 
Black  lays  down  as  a  sine  (p.m  non.  of  a  gland  that  there  should 
be  an  oj)ening  to  the  surface.  He  has  made  an  attempt  (Fig.  15) 
to  demonstrate  such  an  outlet,  but  this  figure  does  not  show 
clearly  that  the  glands  empty  into  the  duct  or  have  an  exit  at 
the  surface.  These  bodies,  however,  not  only  fail  (like  the 
ductless  glands)  in  this  particular,  but  in  more  important 
characteristics  of  glands.  They  do  not  have  (as  Robin  and 
IMagitot  remark)  a  columnar  or  prismatic  cell  wall.  It  is  not 
difficult  to  understand  how  epithelial  cells  are  scattered  in  dif- 
ferent shapes  and  sizes  throughout  the  peridental  membrane. 
Epithelial  cells  have  the  property  of  multiplying  and  develop- 
ing in  structures  wherever  located." 

If  epithelial  cells  should  migrate  within  the  submucous  mem- 
brane and  fibrous  tissue,  proliferation  will  occur  under  certain 
circumstances.  The  tooth,  according  to  Minot,^  is  a  papilla 
which  projects  into  the  epidermis  and,  ossifying  (calcifying)  in  a 
particular  way,  changes  into  ivory  around  the  soft  core  or  pulp  ; 
to  the  papilla  the  epidermis  adds  a  layer  of  enamel.  The  tooth 
proper  unites  with  a  small  plate  of  dermal  bones  at  its  base.  By 
a  modification  in  the  jaws  the  epidermis  first  grows  into  the  der- 
mis and  then  the  dermal  tooth  papilla  is  develoj)ed.  The  first 
indication  of  the  develo23ment  of  tooth  germs  in  mammals  is  a 
thickening  of  the  epithelium  covering  the  jaw.  This  thickening, 
which  appears  as  a  ridge  during  the  sixth  week  of  embryonic 
life,  forms  on  the  under  side  of  the  ejDithelium.  This  curving 
ridge  expands  into  an  outer  portion  (the  outline  of  the  groove 
between  the  lip  and  the  gum)  and  an  inner  portion,  the  dental 
shelf  which  grows  obliquely  inward.  The  papillae  for  the  milk 
teeth  are  formed  on  the  under  side  of  the  shelf,  and  it  is  thus  - 
possible  for  the  shelf  to  continue  growing  toward  the  lingual 


'  Dental  Cosmos,  February,  1899,  pages  112-118. 
-Dental  Follicle,  page  116. 
'  Embryology,  pages  581-90. 


54  INTERSTITIAL    GINGIVITIS. 

side,  so  that  the  second  set  of  germs  is  develoj^ed  for  tlie  perma- 
nent teeth.  The  end  of  the  shelf,  toward  the  articulation  of  the 
jaws,  is  prolonged  without  retaining  the  direct  connection  with 
the  ej^ithelium  and  from  this  jji'olongation  arise  the  enamel 
organs  for  the  three  permanent  molars.  Wherever  a  tooth-germ 
arises  the  dental  shelf  is  locally  enlarged,  and  the  local  enlarge- 
ment constitutes  an  enamel  organ  which  projects  from  the  under 
side  of  the  shelf.  The  portions  of  the  shelf  between  the  enamel 
organs  gradually  break  up,  forming  first  an  irregular  network, 
and  later  sej^arate  fragments '  which  may  persist  throughout 
life  and  lead  to  various  pathological  structures.  While  the  per- 
manent germs  are  forming,  the  shelf  is  solid  between  them, 
although  it  has  assumed  the  reticulate  structure  between  the 
germs  of  the  milk  teeth.  In  consequence  of  the  reticular  forma- 
tion, the  fully  developed  enamel  organs  have  several  bands  or 
threads  by  which  they  are  connected  with  the  dental  shelf  jirojier. 

After  the  shelf  has  developed  somewhat,  its  line  of  connection 
wdth  the  ejjithelium  of  the  gum  becomes  marked  by  a  superficial 
groove,  as  may  be  seen  in  the  human  embryo  of  eight  to  ten 
weeks.  This  groove  was  formerly  supjjosed  to  be  the  first  trace  of 
the  dental  shelf,  but  Rose's  observations  correct  the  supposition. 

The  second  step  in  mammals  is  the  formation  of  outgrowths 
(in  man  ten  in  each  jaw)  from  the  under  side  of  the  dental  shelf; 
each  outgrowth  is  the  outline  of  an  enamel  organ  for  a  milk 
tooth.  The  outgrowth  is  covered  toward  the  mesoderm  by  a  layer 
of  the  epidermis,  while  the  core  is  filled  with  polygonal  cells 
which  resemble  those  of  the  middle  part  of  the  Malpighian  layer 
of  the  skin.  The  outgrowths,  after  penetrating  a  short  distance, 
expand  at  the  lower  ends,  but  remain  each  connected  by  a  nar- 
row neck  with  the  oveidying  ei^idermis.  The  expanded  end  is 
the  enamel  germ  proper  ;  it  very  soon  assumes  a  triangular  out- 
line, as  seen  in  sections,  owing  to  the  flattening  of  its  under  side, 
and  at  the  same  time  it  moves  somewhat  toward  the  lips.  Mean- 
while the  shelf  continues  growing  on  the  lingual  side  of  each 
ingrowth  to  j^roduce  the  enamel  organs  destined  for  the  second 
or  permanent  teeth. 

At  this  stage  it  is  noticed  that  the  mesenchyma  under  the 
flattened  end  of  the  enamel  organ  has  become  more  dense,  to 

'  Including  the  epithelial  debris  of  Robin  and  Magitot. 


TRANSITORY    STRUCTURES.  55 

form  the  outline  of  the  dental  papilla,  and  is  beginning  to  develop 
fibrilla?  around  both  the  enamel  germ  and  the  papillary  outline. 
The  fibrillar  envelope  is  the  future  dental  follicle. 

The  third  step  is  a  final  differentiation  of  the  enamel  organ 
and  the  accompanying  shaping  of  the  papilla.  The  enamel 
organ  continues  growing  and  becomes  concave  on  its  under  side 
so  that  the  mesoderm  underneath  acquires  the  shape  of  the 
papilla.  It  is  now  that  the  form  of  the  tooth  is  determined  by 
the  form  assumed  by  the  papilla,  which  in  its  turn  is  prol^ably 
determined  by  the  growth  of  the  enamel  organ. 

The  follicle  is  merely  an  enveloj^e  of  connective  tissue  in 
which  can  be  distinguished  an  outer  dense  and  inner  looser 
layer ;  in  the  latter  the  cells  are  more  distinct  and  the  fibrillte 
are  less  numerous  than  in  the  former.  A  rich  network  of  capil- 
lary vessels  is  developed  in  the  follicle  and  apj^ears  in  part  as  a 
series  of  villous-like  growth  into  the  enamel  organ.  The  follicle 
develops  first  over  the  lower  part  of  the  papilla,  then  over  the 
enamel  organ,  the  neck  of  which  aborts  and  the  follicle  closes 
over,  comj)letely  separating  the  enamel  organ  from  its  parent 
epidermis.  The  enamel  organ  changes  greatly  in  ajjj^earance. 
The  layer  of  cylinder  cells  is  well  preserved  over  the  concave 
surface,  but  only  where  the  epithelium  is  in  contact  with  the  den- 
tal papilla.  In  the  neck  the  cells  become  irregular  in  form. 
Over  the  convex  surface  the  cells  become  lower  and  cul)oidal. 
They  ultimately  atrophy  and  flatten  out.  The  cells  in  the  center 
of  the  enamel  organs  undergo  a  peculiar  metamorphosis.  They 
remain  united  together  b}^  a  few  thread-like  processes. 

It  is  obvious  from  these  changes  in  the  embryo  how  what 
Robin  calls  the  epithelial  debris  is  derived  from  the  epithelial 
cord,  the  follicular  wall  and  the  round  bodies  of  lamina  epithel- 
ium debris.  According  to  Ch.  Robin  and  Magitot,^  who  were 
the  first  to  describe  these  bodies,  "The  phenomena  of  budding- 
commences,  namely,  when  the  epithelial  cord  has  finished  its 
course,  having  conducted  the  primary  enamel  organ  to  that  point 
Avhence  its  subsequent  evolution  will  be  effected  and  soon  after 
the  formation  of  the  secondary  follicle,  immediately  after  the 
rupture  of  the  cord  of  the  primitive  follicle."     Robin  leans  to 

'  See  their  Memoir  on  the  Genesis  and  Development  of  the  Dental  Follicle  in 
Jour,  de  Physiologie  de  Brown-Sequard,  1860. 
5 


56  INTERSTITIAL    GINGIVITIS. 

the  opinion  tliat  these  bodies  disappear  soon  after  they  are 
formed,  "  The  time  of  their  disappearance  varies,  they  remark^ 
in  different  species  of  animals.  In  the  human  embryo  the 
remains  of  the  cord  of  the  primitive  follicles  may  be  fonnd,  even 
after  the  formation  of  the  follicles  of  the  permanent  teeth,  and 
it  is  j)robably  during  the  process  of  eruption  that  these  bud- 
dings become  atrophied ;  in  the  canine  embryo  the  facts  are 
nearly  the  same ;  in  the  bovine  and  ovine  embryos  (calf  and 
lamb)  it  has  seemed  to  us  that  these  proliferations  disappear  at  a 


-__^^_^^^,/  I 

Fig.  24. — Section  through  the  Incisive  Portion  of  the  Lower  Jaw  of  an  Ovine 
Embryo,  Measuring  82  Millim-  (3 J  Inches)  in  Length.  Magnified  260  Diaji., 
after  Dhs.  Ch.  Legros  and  E.  Magitot.  ■ 

D,  Oral  Epithelium.  C,  Lowest  Laj'er  of  Cells  in  the  Stratum  Malpighii. 
F,  Epithelial  Cord.  K,  Bourgeon  of  the  Secondary  Cord.  I,  Follicular  AVall. 
H,  Dental  Bulb. 

correspondingly  earlier  stage ;  and  we  think  it  safe  to  say  that, 
as  a  general  rule,  the  complete  absorption  occurs  toward  the 
period  of  erujstion." 

The  embryology  of  the  dental  shelf,  which  has  been  sum- 
marized by  Minot  from  Waldeyer,  KoUiker,  Von  Ebner'  and 
O.  Hertwig,  indicates  the  source  of  the  structures  which  have 
been  mistaken  by  Black  for  the  limiting  walls  of  glands. 

'  Handbuch  der  Zahnheilkunde,  1890,  pages  209-262. 


TEANSITOKY    !^TRUC'TURE8.  57 

After  the  epithelial  cordis  of  the  temporary  and  permanent 
sets  of  teeth  have  been  demarcated  from  their  follicles,  the  proc- 
ess of  cell  building  proceeds  like  the  process  of  cord  building. 
These  buds,  according  to  Charles  Robin  and  Magitot,'  are  given 
oif  at  the  upper  border  of  the  follicle  and  below  the  ejjithelium 
of  the  gum.  "  In  fact,  as  soon  as  the  epithelial  lamina  loses  its 
connection  with  the  follicle,  by  the  rupture  of  the  cord,  the  epi- 
thelial cells  composing  it  become  greatly  increased  in  number  at 
the  severed  point.     The  multip)lication  of  cell-elements  results 


ji|@ 


Fig.   25. — Vertical   Tr.vnsversb   Section   through   the   Ixcisive    Region    of   the 
Lower  Jaav  of  Ho.ai.^s  Foltits  Measurixg  38  Centimetres  (15}  Inches),  M.-iG- 

NIFIED   80   DiAM.,    AFTER   DrS.   Ch.   LeGROS   AND   E.    MaGITOT. 

b,  Bony  Formation.  d,  Oral  Epithelium.  g,  Enamel  Organs.  H,  Dental 
Bulb.  I,  Cord  of  the  Permanent  Follicle.  K,  Debris  on  the  Follicular  Wall  of  the 
Primitive  Follicle  and  from  its  Cord.  K,  E[jithelial  Globule.  L,  Enamel  Organ  of 
the  Permanent  Tooth. 

in  the  formation  of  irregular  buddings,  which  wander  in  different 
directions  into  the  deeper  portions  of  the  embryonal  tissue. 
These  buddings  vary  greatly  in  form  ;  sometimes  they  are  sim- 
ple cylinders,  retaining  their  connection  with  the  primitive 
lamina  by  pedicles  of  various  lengths,  and  sometimes  this  slight 
connective  is  absorbed,  thus  isolating  an  ejjithelial  mass." 

This  budding  occurs  at  different  points  along  the  cord  (Fig. 
24)  at  the  end  and  upon  the  outer  surface  of  the  follicular  wall 
(Figs.  25  and  2B)  at  the  point  where  the  cord  is  severed  from  the 

'Loc.  cit.,  1860. 


58    ■  IXTEESTITIAL    GIXGIVITIS. 

enamel  organ.  These  gradually  diminish  as  they  descend  upon 
its  sides.  Doubtless  the  epithelial  cord  remains  in  the  periosteal 
and  submucous  tissue  throughout  life.  Fig.  27  represents  evident 
sections  of  epithelial  cord  in  a  man  sixty-eight  years  of  age,  and 
Fig.  28  in  a  dog  eight  years.  In  the  photographs  of  the  scurvy 
cases  and  of  dogs  will  be  seen  evidences  of  the  persistence  of 
epithelial  debris  late  in  life.     The  position  already  cited  from 


^WM^S'M 


,.-.    V 


Fig.  26. — Fkoji  the  Loiver  Jaw  of  ax  Ovine  Embryo,  Magnified  80  Diameters, 
Showing  the  Completed  Dental  Follicle  and  the  Surrounding  Tissues, 
after  Drs.  Ch.  Legros  and  E.  Magitot. 

a,  Meckel's  Cartilage.  b,  Traces  of  Ossification,  c,  Lowest  Layer  of  Epithelial 
Cells,  d,  Oral  Epithelium.  F,  Ameloblastic  Layer.  F,  (Lower)  External  Layer  of 
the  Enamel  Organ — a  continuation  of  the  Layer, of  Ameloblasts.  g,  Stellate  reticu- 
lum of  the  Enamel  Organ.  H,  Bulb.  I,  Follicular  Wall.  K,  Buddings  from  the 
Cord. 

Hobin  and  INIagitot  as  to  its  early  disappearance  would  hence 
apj^ear  to  be  too  strongly  taken. 

Robin  and  ^lagitot  claim  that  this  budchng  jjrocess  occurs  at 
or  about  the  time  of  the  rupture  of  the  cord.  Up  to  this  period 
ossification  has  not  taken  place,  but  then  deposits  of  bone  ap]3ear 
in  the  fibrous  tissue  of  the  middle  and  outer  surfaces.  The  bone 
dej^osit  gradually  takes  the  form  of  the  jaw,  filling  in  and 
encroaching  upon  the  fibrous  tissue,  forming  a  Ijony  wall  on  the 


TKANSITORY    STRUCTURES. 


59 


one  hand,  and  the  crown  and  root  of  the  tooth  on  the  other. 
When  the  tooth  is  ready  to  erupt,  the  crown  pushes  the  soft  tissue 
hiterally,  while  the  root  develops,  forms  a  defined  wall  with  the 
peridental  membrane  between  them.  The  epithelial  debris  (to 
use  their  term)  which  before  was  scattered  over  the  entire  surface 
of  the  dental  follicle,  is  now  crowded  into  the  very  narrow  space 


X  50.    One-half-in.  obj.    No,  Oc. 

Fig.  27. — Cross  Section  of  Epithelial  Cord.    M.\x. 

I,  Peridental  ^Membrane.    W,  Epithelial  Debris  or  Cord.    EO,  Endarteritis  Obliterans. 

of  the  peridental  membrane,  and  owing  to  the  position  of  the 
debris  at  the  upper  part  of  the  follicle,  it  would  be  natural  to  find 
most  of  it  at  the  peridental  membrane. 

BONE   BUILDING    AND    ABSORPTION. 

Development  of  the  alveolar  process  is  relegated  to  a  series 
of  cells  situated  in  the  fibers  of  the  peridental  membrane  or 
fibrous  tissue,  and  close  to  the  maroin  of  the  bone  tissue,  and 


60 


INTERSTITIAL    GINGIVITIS. 


tliroughout  the  Haversian  canals.  These  cells  are  called  the 
osteoblasts.  They  perform  the  function  of  building  up  the  bone 
tissue.  Even  after  the  alveolar  process  has  developed  its  normal 
shape,  so  unstable  is  the  nervous  system  which  presides  over 
these  cells  at  this  locality,  that  at  the  slightest  provocation,  either 


X  5fi0.    No.  2  projection  ocular.    One-t^\'elfth  obj.     Zeiss. 

Fig.  28. — Cross  Section  Epithelial  Cokd.     Dog. 

I,  Peridental  Membrane.     W,  Epithelial  Debris  or  Cord.    U,  Nerve  Tissue. 

local  or  constitutional,  they  will  continue  their  process  of  con- 
struction. Hence,  the  frequency  of  hyperti-ophy  of  the  process, 
and  in  disease  the  calcification  of  the  j^eridental  membrane. 

On  the  other  side  of  the  membrane,  next  the  root  surfaces, 


TRANSITORY    STRUCTURES.  61 

may  be  seen  other  cells  Avliicli  l^uild  up  aucl  destroy  the  cemen- 
tum;  these  are  called  cemeutoblasts  and  cementoclasts.  These 
are  of  little  importance  in  this  connection  with  the  study  of  this 
disease,  although  they  are  frequently  present  and  at  work  when 
inflammation  of  the  membrane  occurs. 

There  is,  however,  another  class  of  cells  found  in  the  2;)eri- 
dental  membrane  of  the  utmost  importance  in  this  connection, 
the  osteoclasts,  located  in  the  fibers,  and  in  close  proximity  to 
the  alveolar  wall,  and  around  the  inner  border  of  the  Haversian 
canals.  The  function  of  these  cells  is  to  tear  down  irregular 
bone  and  tooth  structure  due  to  unstal:»le  nervous  tissue,  and  from 
the  slightest  irritation. 

The  gums,  mucous  membrane,  alveolar  process  and  peridental 
membrane,  owing  to  their  transient  nature,  are  influenced  by  the 
slightest  irritation.  This  influence  is  the  result  of  both  constitu- 
tional and  local  causes.  It  consists  of  an  irritation  in  the  periph- 
eral nerves  which  sets  the  osteoblasts  and  osteoclasts  at  work 
to  build  up  or  tear  down  the  alveolar  process.  This  influence 
may  be  only  sufficient  to  stimulate  these  cells  to  action  without 
inflammation.  This  is  noticed  in  the  advance  toward  old  age,  in 
long,  lingering  debility,  in  the  development  of  bone,  especially 
the  tearing  down  and  the  building  up  of  the  inferior  maxillary 
backward.  It  may  be  noted  in  mild  or  intense  iuflanimation  of 
the  peridental  membrane,  due  to  more  acute  forms  of  disease,  to 
scurvy,  mercurial,  lead  and  iodide  poisoning,  or  to  local  irrita- 
tion. So  sensitive  are  these  structures  that  in  neurotics  and 
degenerates  the  slightest  irritation  produced  in  the  physiologic 
development  of  the  permanent  teeth  is  sufficient  ■  to  start  the 
osteoblasts  to  building  up  bone  structure,  thus  producing  that 
pathologic  condition  called  hypertrophy  of  the  alveolar  process ; 
one  of  the  most  marked  evidences  of  an  unstable  nervous 
system. 

The  breaking  down  of  the  tissues  by  the  osteoclasts  nuiy  lie 
induced  by  as  slight  a  cause.  The  alveolar  process  being  so  thin 
about  the  teeth,  destruction  of  the  entire  walls  is  accomplished 
without  difficulty,  and  in  a  very  short  time,  thus  loosening  the 
teeth,  which  eventually  drop  out. 

According  to  Kaufmann'  the  following  processes  take  part  in 

'  Pathologische  Anatomie. 


62 


INTERSTITIAL   GUNGIVITIS. 


the  absorption  of  bone :  (a)  Lacunar  Absorption,  (b)  Forma- 
tion of  Perforating  Canals,  (c)  Disappearance  after  Prior 
Absorption  of  Lime  (Halisteresis)  (Bony  Waste)  and  Osteo- 
malacia. 

"By  far  the  commonest  form  of  bone  destruction  is  by  lacunar 
absorjDtion.  This  process  occurs  not  only  under  physiologic 
conditions,  but  is  extraordinarily  frequent  in  pathologic  states, 
e.  g.,  in  the  various  types  of  atrophy.  They  form  on  the 
smooth,  su]jerficial  surfaces  of  the  bone  deep  grooves  (so-called 
Howship's  lacunae)  in  which  lie  smaller  or  greater  polynuclear 
cells  (osteoclasts,  Kolliker)  which  evidently  blend  together  (Fig. 
29).     There  are  no  alterations  of  the  bone  substance  that  would 


^^^^if^0^P^^^^^^'^'^-%^' ' 


^^^m- 


a,  Bone  Trabecule,      b,  Tubercle  with  Granulation  Tissue,      c,  Broken-down  Tissue. 
d,  Blood  Vessel,    e,  Osteoclasts.    /,  Fat  Cells. 

indicate    a   jarimary  line  of  absorption   (Plummer).     The  con- 
fluence of  these  lacunae  form  larger  cavities. 

"  The  second  form  of  bone  absorjDtion,  which  is  occasionally 
met  under  physiologic  conditions,  is  by  means  of  perforating 
canals  (so-called  Volkmann  canals).  Under  physiologic  condi- 
tions canals  occur  in  varying  numbers  in  the  lamellse  (general 
lamellae)  which  contain  vessels  (perforating  vessels).  These  are 
often  associated  with  the  Haversian  canals  and  gradually  pass 


TRANSITORY    STRUCTITRES. 


63 


into  them,  but  unlike  tliem,  are  surrounded  witli  circular  1am- 
ellee.  Under  ^^athologic  conditions  the  conception  of  these  j^er- 
forating  canals  is  somewhat  widened.  On  the  one  hand 
Volkmann's  canals  are  spoken  of  when  reference  is  made  to  the 


b     a  e  c 


a,  Large  Spaces  Resulting  from  Absorption  of  the  Trabecule.      6,  Decalcified  Bone, 
c  and  d,  Decalcified  Bone  and  Atrophied  Trabecuhe.        e.  Haversian  Canals. 


vessels  or  vascular  connective  tissue  penetrating  from  one  medul- 
lary space  in  the  spongy  substance,  or  from  one  Haversian  canal 
in  the  comjiact  substance,  to  another,  in  such  a  way  that  a  passage 
is  made  from  one  part  of  the  bone  to  the  other ;  Volkmann's- 
canals  also  include  irregular  ampula-formed  dilations  or  cavities- 


•64  INTEESTITIAL    GINGIVITIS. 

(Fig.  30).  By  confluence  of  these  are  j^i'oclucecl  cavities  or  irreg- 
ularly outlined  canals  penetrating  the  bone  substance.  These,  if 
they  emj^ty  into  the  medullary  space,  become  filled  with  cells. 

"  Under  much  rarer  conditions,  especially  in  senile  marasmic 
osteomalacia  and  also  in  that  occurring  in  pregnancy,  bone 
absorption  takes  place  after  a  prior  abstraction  of  lime  (halister- 
esis)  and  the  remaining  substance  (bone  cartilage)  is  then  further 
■dissolved,  passing  through  a  temporary  fibroid  stage.  This 
destruction  of  the  decalcified  and  interfibrillse  decomposed  bone 
is  produced  as  a  rule  without  osteoclasts.  The  decalcified  border 
zones  of  the  trabeculse  appear  with  sim^jle  carmine  (coloring)  or 
by  double  stains." 


CHAPTER  IV. 

THEORIES    OF    INTERSTITIAL    GINGIVITIS. 

The  etiology  of  interstitial  gingivitis,  according  to  the  views 
summarized  previously,  is  divisible  into  local  and  constitutional. 
While  one  school  leans  largely  to  the  local  etiology,  another 
advocates  as  strongly  the  constitutional  theory.  In  a  general 
way,  etiology  may  be  divided  into  exciting  and  j)redisj)Osing. 
Etiology  may  also  dej^end  ujjon  an  element  dependent  on  the 
exciting  cause,  an  element  dependent  on  the  constitution  of  the 
individual  attacked,  and  finally  an  element  dependent  on  his 
condition  when  attacked,  both  as  regards  his  general  system 
or  any  one  of  his  organs.  The  chief  constitutional  causes  to 
which  the  disease  has  been  ascribed  are  general  conditions  of  the 
health,  heredity,  constitutional  disorders,  excessive  lime  salt 
secretion,  meat-eating,  nervous  exhaustion,  scorbutus  and  uric 
acid  states,  as  well  as  environment.  The  local  causes  assigned 
are  acute  inflammation  of  the  mucous  membi'anes,  catarrhal 
states,  germs  or  fungi,  irregular  teeth,  lactic  acid,  jDOcket  dis- 
ease, hfemorrhagic  deposits,  serumal  calculi  and  uncleanliness. 
That  all  these  factors  exercise  an  influence  is  undeniable,  but 
the  enormous  etiologic  role  which  has  been  assigned  to  some  of 
them  is  the  result  of  generalization  from  too  few  cases.  Many 
■of  the  assigned  causes  could  lie  comjiressed  into  fewer  etiologic 
influences.  Thus  meat-eating  and  the  uric  acid  states  are  too 
intimately  connected  to  be  regarded  as  different  causes,  from  a 
constitutional  standpoint.  As  has  been  already  pointed  out,  uric 
acid  acts,  when  it  acts  at  all,  like  lactic  and  other  acids,  as  a  local 
irritant  rather  than  as  the  constitutional  condition  (as  many  sup- 
pose) which  underlies  its  production  and  of  which  it  serves  as  an 
index. 

Scorbutus  is  an  expression  of  a  nutritional  disorder  due  very 
frequently  in  the  adult  to  an  excess  of  meat  or  a  monotony  of 
diet.  It  is  a  constitutional  disorder,  peculiarly  apt  to  have  its 
local  expression  in  the  gums  long  ere  the  general  constitutimial 


66  I^TTEESTITIAL    GINGIVITIS. 

symptoms  are  manifest.  The  germs  and  fungi  etiologists,  on  tlie 
other  hand,  tend  to  ignore  the  constitutional  state  behind  the 
local  culture  medium,  which  must  be  furnished  before  growth  of 
the  germ  or  fungus  can  occur.  In  order,  therefore,  to  determine 
whether  an  alleged  cause  be  exciting  or  ^predisposing  and  what 
is  the  influence  of  the  etiologic  moment,  as  the  union  at  one  time 
of  the  two  constitutional  factors  already  cited  is  called,  analysis 
is  required  of  all  the  varied  factors  charged  with  producing  the 
disease.  The  influence  of  heredity  is  generally  left  out  of  con- 
sideration unless  it  be  direct,  which  it  rarely  is,  since  heredity, 
as  has  been  w^ell  remarked,  is  usually  a  prophecy  rather  than  a 
destiny.     It  hence  constitutes,  as  a  rule,  a  predisposition. 

The  chief  tissues  concerned  in  the  elimination  of  waste  jDrod- 
ucts  are  the  skin,  the  lungs  and  air  passages,  including  the 
mouth  and  nose,  the  kidneys,  liver  and  intestines.  Interference 
with  the  eliminatory  powers  of  the  kidneys,  liver  and  intestines 
is  especially  apt  to  throw  extra  work  on  the  skin,  lungs  and  air 
passages.  Of  this  a  sour-winey  odor  of  the  breath  in  diabetes  is- 
an  excellent  illustration.  What  is  true  of  such  a  marked  form 
of  suboxidation,  resulting  in  auto-intoxication,  is  true  of  less 
pronounced  forms.  The  peculiarly  foul  odor  of  the  breath  and 
skin  in  feecal  intoxication  indicates  that  the  mucous  membranes 
of  the  nose,  throat,  mouth  and  gums  are  doing  the  work  of 
elimination  which  should  have  been  done  by  the  intestines. 
The  failure  of  the  kidney  to  perform  its  share  of  eliminatory 
work  is  most  apt,  however,  to  find  expression  in  the  skin,  lungs,, 
nose,  mouth  and  gums. 

The  influence  of  the  nervous  system  on  the  growth  and 
repair  of  any  tissue  is  admitted  by  every  physiologist.  This- 
influence  is  entitled  the  trophic  function  of  nerves.  It  is  not, 
however,  exactly  settled  whether  it  be  exerted  through  the 
nerves  themselves  or  secondarily  through  their  control  of  the 
vaso-motor  (blood  vessel)  system.  Many  trophic  disturbances,, 
as  J.  Collins  ^  remarks,  are  j)robably  due  to  vaso-motor  changes,, 
and  it  is  not  possible  to  separate  by  any  sharjjly  deflned  line  the 
vaso-motor  from  the  trojjho-neuroses.  At  the  same  time,  it 
should  be  distinctly  remembered  that  there  exist  troj)ho-neuroses 
in  which  there  are  no  appreciable  vaso-motor  change  as  in  many 

'  Nervous  Diseases,  by  Dr.  F.  X.  Dercum. 


THEOEIEf!!    OF    INTEESTITIAL    GINGIVITIS.  67 

cases  of  acromegaly  and  hypertrophies.  On  the  other  hniul, 
there  are  any  amount  of  vaso-motor  disturbance  which  are  ))y 
no  means  trophic  in  character.  Trophic  disturbance,  which  may 
play  a  very  important  part  at  the  onset  of  interstitial  gingivitis, 
is  neurotic  oedema  due  to  nerve  irritation.  While  this  is  most 
frequent  on  the  face,  lips,  tongue,  pharynx,  forehead  and  genital 
organs,  it  also  apj^ears  on  the  gums.  The  oedema  reaches  its 
full  development  from  one-half  to  two  hours.  There  is  a  feeling 
of  stiffness  and  unyieldingness,  but  no  sensation  of  inflammatory 
swelling.  This  type  of  trophic  disorder  often  initiates  changes 
in  the  mucous  membrane  which  may  readily  form  the  basis  of 
interstitial  gingivitis.  This  condition  may  not  be  only  due  to 
ordinary  nervous  causes,  but  may  arise  from  constitutional  con- 
ditions, gout,  etc.,  and  toxic  influences. 


CHAPTER  V. 

URIC  ACID  AND    INTERSTITIAL   GINGIVITIS. 

Wliat  John  Fitzgerald'  calls  tlie  giagival  organs,  possess,  as- 
lie  remarks,  in  common  with  some  other  tissues  of  the  body,  the 
power  of  selecting  and  excreting  poisonous  substances  from  the 
blood.  Some  of  these  cause  hyperfemia,  or  even  inflammation,  in 
their  passage.  Uric  acid  has  been  found  to  play  a  part  in  so 
many  excretions  that  it  has  naturally  attracted  attention  here. 
The  trend  of  medical  opinion  has  set  strongly  in  this  directioUr 
but  of  late  this  trend  is  changing. 

During  the  past  two  decades  uric  acid  has  assumed  again  the 
j)rominence  in  pathogeny  which  it  once  had  when  called  sup- 
pressed gout.  It  is  not  surprising,  therefore,  to  find  that  Reeves, 
Pierce,  Kirk,  Rhein  and  others  claim  a  uric  acid  etiology  for 
interstitial  gingivitis.  In  support  of  this  claim  are  advanced  the 
results  of  three  experiments  which  Pierce  has  had  made  on 
tooth  deposits.  These  deposits  were  examined  chemically  by 
Ernst  Congdon,  of  the  Drexel  Institute.'  The  first  specimen 
contained  a  number  of  needle  crystals  of  calcium  urate,  a  few 
crystals  of  free  uric  acid  and  crystals  of  calcium  jjhosphate. 
Destructive  distillation  gave  a  strong  ammonic  reaction.  The 
murexid  test  for  uric  acid  and  its  compounds  gave  faint  results, 
although  its  characteristic  color  was  evident  in  several  places. 
The  second  specimen  presented  the  same  crystals.  The  reaction 
to  the  murexid  test  was  strong  and  resulted  in  a  number  of 
purplish-red  spots.  Similar  results  were  obtained  from  the  third 
specimen.  A.  B.  Brubaker  examined  six  or  eight  specimens 
in  Pierce's  presence,  with  like  results  to  those  obtained  in  the 
previous  examination.  In  three  an  abundance  of  sodium  urate 
crystals  was  present. 

The  great  deficiency  in  the  experiments  thus  described  is  the 
small  number  of  cases  examined  and  the  lack  of  proper  control 

^  The  Clinical  Journal,  March  1,  1899. 

-International  Dental  Journal,  Vol.  XV,  pages  1,  217,  501. 


UEIC    ACID    AND    INTERSTITIAL    GINGIVITIS.  G9" 

experiments.  These  elements  have  so  frequently  led  to  errors  in 
dental  pathology  that  I  determined  upon  a  series  of  investigations 
in  two  different  laboratories,  whose  results  were  rej)orted  some 
years  ago.^  The  Columbus  Medical  Laboratory  was  selected  for 
one  series  of  experiments  in  special  cases.  The  laboratory  of  the 
Northwestern  University  Woman's  Medical  School  was  selected 
for  the  other  series  of  experiments,  to  which  teeth  were  sent  as 
soon  as  they  were  obtained.  One  hundred  and  fifteen  teeth  were 
sent  to  the  laboratory  last  named  from  three  institutions  in 
Chicago  which  make  a  specialty  of  extraction.  These  teeth  liad 
no  history  other  than  the  fact  that  the  cases  were  well-marked 
instances  of  interstitial  gingivitis  with  plenty  of  calcic  deposits, 
and  that  the  teeth  were  loose  in  the  sockets  when  extracted.  Of 
the  one  hundred  examinations  made  in  the  Columbus  Medical 
Laboratory,  fifty  were  upon  specimens  of  calcic  deposits  from  my 
patients  and  fifty  were  upon  sjDecimens  obtained  from  the  institu- 
tions just  mentioned,  and  were  therefore  without  history.  The 
tests  employed  were  the  hydrochloric  acid,  the  dry  distillation, 
and  the  nuirexid,  these  being  the  tests  recommended  by  Pierce. 
The  examinations  in  the  Columbus  Medical  Laboratory  were 
made  by  J.  A.  Wesener,  and  those  in  the  laboratory  of  the 
Northwestern  University  Women's  Medical  School  by  J.  H. 
Salisbury. 

Of  the  one  hundred  and  fifteen  examinations  made  at  the 
Northwestern  University  Woman's  Medical  School  by  the  first 
test,  in  only  two  cases  was  found  the  needle-shaped  crystals,  and 
one  in  Avhich  there  Avas  a  slight  resemblance  of  uric-acid  crystals. 
By  the  dry  distillation  test,  thirteen  gave  no  reaction  from 
ammonia,  and  in  seven  the  reaction  was  slight.  The  remaining 
eighty  gave  a  decided  reaction.  By  the  murexid  test,  four  gave 
a  slight  murexid  color,  but  remainder  gave  no  reaction.  Special 
examination  was  made  of  twelve  of  these  teeth  by  the  addition 
of  strong  hydrochloric  acid,  warming,  decanting  the  acid,  and 
washing  with  water.  These  gave  no  reaction  by  the  dry  distilla- 
tion tests  for  ammonia.  Two  gave  a  slight  reaclfion  by  the 
murexid  test.  In  examination  of  the  teeth  of  three  uric-acid 
diathetic  women,   over  forty   years  of   age,   uric   acid  was  not 

'Dental  Cosmos,  April,  1896,  page  310.  Journal  of  the  American  Medical  Asso- 
ciation, January  16,  1S97. 


70  INTERSTITIAL    GINGIVITIS. 

detectible  either  by  the  niurexid  test  or  microscopically.  The 
examinations  made  in  the  Columbus  Medical  Laboratory  were 
still  more  interesting,  since  among  them  were  specimens  from 
patients  whose  history  could  be  obtained.  Of  the  fifty  obtained 
outside,  eight  gave  positive  results  from  all  three  tests.  The 
other  forty-two  were  positive  by  dry  distillation,  and  negative  by 
the  murexid  and  microscopical  tests.  Of  the  fifty  patients, 
thirty-eight  females  and  twelve  males,  thirty-two  were  over  forty 
years  of  age,  twelve  over  thirty  years,  and  six  over  fifteen  years. 

Twenty-six  have  uric  acid  to  a  greater  or  less  extent,  nine 
suffer  with  indigestion,  seven  of  which  are  subject  to  sick  head- 
ache, thirty-four  have  rheumatism.  Six  are  English,  and  four  of 
these  have  the  true  gout ;  the  other  two  have  rheumatism. 

All  are  j^ositive  with  the  dry  distillation  test.  All  are  nega- 
tive Avith  the  murexid  test.  Forty-nine  are  negative  with  the 
microscopical  test.  One  shows  needle-shaped  crystals,  but  not 
uric  acid.  It  is  a  singular  fact  that  in  both  laboratories,  the 
cases  in  which  there  was  uric  acid  and  gouty  histories  gave  nega- 
tive results.  By  the  dry  distillation  test,  out  of  two  hundred 
and  fifteen  cases,  all  but  twelve  cases  (which  have  been  treated 
to  remove  nitrogenous  material)  responded.  The  twelve  cases  so 
treated  did  not  respond,  since  nitrogenous  compounds  in  and 
about  teeth  (even  the  saliva)  burned  to  an  ash  will  jDroduce 
ammonia.  By  the  murexid  test  only  twelve  out  of  the  two 
hundred  and  fifteen  gave  a  jDOsitive  reaction.  By  the  micro- 
scopic examination  but  ten  showed  crystals.  One  of  the  chemists 
who  made  the  examination  is  positive  that  they  were  uric  acid 
crystals.  The  other  is  not,  since  lime-phosphate  crystals  resemble 
uric  acid  crystals  too  minutely  to  be  distinguished  positively. 

For  three  years  Wesener  made  further  examinations  as  to  the 
relative  value  of  the  three  tests  employed.  According  to  his 
experiments  the  murexid  test  is  the  most  valuable,  the  crystal 
test  second,  and  the  dry  distillation  third.  The  murexid  test  is 
the  most  reliable  in  testing  tartar  for  uric  acid,  since  its  red  color 
is  easily  distinguished  from  other  colors  and  the  test  is  simple  in 
ap2:)lication.  The  test  for  crystallized  uric  acid  is  very  unsatis- 
factory, since  here  must  be  dealt  with  a  complex  mass  which  not 
only  contains  crystals  of  calcium  phosphate  (very  similar  to  those 
of  uric  acid)  but  a  great  mass  of  detritus  obscuring  the  crystals 


URIC    ACID    AND    INTERSTITIAL    GINGIVITIS.  71 

of  uric  acid.  If  crystals  be  present  they  by  no  means  settle  the 
existence  of  uric  acid.  When  the  faintest  quantity  possible  of 
uric  acid  is  mixed  with  tartar  from  teeth  and  subjected  to  crystal- 
lization, the  results  are  always  negative.  If  subjected  to  the 
murexid  test,  the  results  are  always  positive.  The  dry  distilla- 
tion test  is  so  inaccurate  as  to  be  unworthy  consideration. 

Since  these  results  were  published,  seven  hundred  and  thirty- 
five  cases  have  been  examined.  These  examinations  were  con- 
ducted by  Jerome  H.  Salisbury,  now  of  Rush  Medical  College. 
The  teeth  procured  from  institutions  which  make  a  specialty  of 
extracting  contained  the  dark  calcic  deposit  above  the  pus  line. 
By  the  murexid  test,  six  out  of  the  three  hundred  gave  a  distinct 
reaction  ;  eighteen  showed  crystals  under  the  microscope.  The 
murexid  test  was  performed  as  follows  :  The  deposit  was  selected 
as  carefully  as  possible,  removed  from  the  tooth,  and  jjlaced  in  a 
small  porcelain  crucible.  A  drop  of  pure  nitric  acid  was  added 
and  the  mixture  evaporated  on  the  water  bath.  AVhen  dry,  the 
evaporation  was  repeated  with  another  drop  of  nitric  acid,  and 
the  crucible  allowed  to  cool.  When  cool,  the  color  produced  by 
the  nitric  acid  was  observed,  and  then  a  glass  rod,  wet  with 
ammonia  water,  was  brought  near  the  deposit,  and  any  color  ^^ro- 
duced  was  noted.  If  no  color  was  observed,  the  ammonia  was 
allowed  to  flow  over  the  residue.  A  j^ellow  color  was  produced 
in  many  cases  by  the  nitric  acid,  which  was  deepened  by  the 
addition  of  ammonia.  The  microscopic  examination  was  made 
by  scraping  off  the  deposit  and  evaporating  it  with  a  drop  of 
hydrochloric  acid.  The  residue  was  moistened  vfith  water,  and 
the  insoluble  material  placed  on  a  slide  and  covered  with  a 
cover-glass.  It  was  examined  with  a  No.  7  objective.  Uric 
acid,  therefore,  occurred  in  a  certain  very  small  proportion  of 
cases  of  calcic  deposit  on  the  teeth. 

Four  hundred  and  thirty-five  cases  were  later  examined,  mak- 
ing in  all  nine  hundred  and  fifty.  Out  of  these  four  hundred 
and  thirty-five  cases  only  four  per  cent  showed  uric  acid  by  the 
murexid  test  and  eight  per  cent  by  the  crystal  test.  Since  the 
crystal  test  is  not  so  accurate  as  the  murexid  test,  it  is  safe  to  say 
that  six  per  cent  was  the  actual  [)er  cent  of  ui'ic  acid.  As  a 
result  of  the  different  experiments,  iu  tlie  first  two  liuudred  and 
fifteen  cases  five  per  cent  uric  acid  was  found.     In  the  second 

G 


72  INTERSTITIAL    GINGIVITIS. 

three  hundred  cases,  four  per  cent,  and  in  the  third  four  hundred 
and  thirty-five  cases,  six  per  cent  was  found.  In  an  examination 
of  nine  hundred  and  fifty  cases  by  different  chemists  at  different 
periods,  five  to  six  per  cent  give  j)Ositive  results  as  to  uric  acid  by 
the  chemic  and  microscopic  examination.  These  results  demon- 
strate conclusively  that  interstitial  gingivitis  is  not  due  solely  to 
uric  acid ;  that  uric  acid  when  found  is  merely  an  expression  of 
the  uric  acid  diathesis  and  a  coincidence,  since  it  is  not  always 
present  in  the  gums  and  tartar  of  patients  attacked  either  by  gout 
or  the  uric  acid  diathesis.  In  the  six  per  cent  of  cases  there  was 
nothing  to  show  that  uric  acid  was  the  cause  of  interstitial  gingi- 
vitis, since  the  deposits  were  examined  after  the  teeth  ha,d  been 
removed.  Any  other  irritation  may  have  been  the  exciting 
cause.     Uric  acid  acts,  when  at  all,  solely  as  a  local  irritant. 


CHAPTER    VI. 

INORGANIC  SALTS  AND  INTERSTITIAL  GINGIVITIS. 

The  foods  which  enable  the  body  to  repair  its  waste,  to  build 
up  new  tissue  and  to  supply  the  energy,  are  divisible  into  four 
classes :  the  inorganic  substances,  the  fats  or  hydrocarbons, 
and  the  starches  and  sugars,  or  carbohydrates,  and  the  proteid 
compounds.  These  divisions  are,  however,  relative,  since  the 
proteids  may  contain  both  hydrocarbons  and  carbohydrates. 
The  inorganic  substances,  such  as  water,  phosphates,  chlorides, 
carbonates,  sulphates,  etc.,  enter  the  body,  as  a  rule,  under  their 
own  form,  either  alone  or  in  combination  with  other  classes. 
They  are  not  oxidized  or  split  up  within  the  system  to  enter  into 
the  chemical  formations  of  other  compounds,  but  are  united 
mechanically  with  the  proteid  group.  These  bodies  act,  as  a  rule, 
in  a  j)urely  mechanical  manner.  After  having  served  their  pur- 
pose, they  pass  out  of  the  system  with  the  excretions,  compara- 
tively unchanged  in  their  composition.  They  are  the  only 
member  of  the  group  of  foods  which  are  of  a  special  interest  in 
the  present  research.  The  inorganic  salts  have,  however,  not 
received  the  attention  from  physiologic  chemists  that  their 
importance  demands.  They  are,  as  a  rule,  found  in  greater  or 
lesser  quantity  in  all  foods  that  are  taken  into  the  body.  They 
do  not  serve  as  a  source  of  energy,  but  as  the  other  foods  are 
needed  for  the  develojjment  of  the  tissues,  so  the  inorganic  salts 
are  needed  for  the  building  of  bone  tissue  and  the  repair  of 
waste.  This  is  accomplished  by  the  soluble  salts  in  the  blood. 
Human  blood  has  the  following  comj)Osition  : 

ANALYSIS  OF  HUMAN  BLOOD  (C.   SCHMIDT).  HOWELL'S 
PHYSIOLOGY. 

Man.  Woman. 

25  Years.  30  Years. 

Water 788.71  ....  824.55 

Solids    211.29  ....  175.45 

Proteids  and  Extractives 191.78  ....  157.93 

Fibrin 3.93  1.91 

HcTsmatin  (and  iron) 7.70  ....  6.99 

Salts 7.88  ....  8.62 


74  INTERSTITIAL    GINGIVITIS. 

INORGANIC  SALTS  OF  HUMAN  BLOOD,    1,000  PARTS 
(C,   SCHMIDT). 


Blood  Corpuscles. 

CI 1.75 

Kjo 3.091 

NAju 0.470 

SOg    0.061 

205   ••••• I.ODO 

CaO 

M<„ 


Blood  Plasma. 

CI 3.536 

Kjo 0.314 

NA2„ 3.410 

SO3 0.129 

P205    0-1^5 

CaO 

M90 


These  acids  and  bases  exist,  of  course,  in  tlie  plasma  and  the 
corpuscles  as  salts.  It  is  not  possible  to  determine  exactly  how 
they  are  combined  as  salts,  but  Schmidt  suggests  the  following 
combination  : 

PROBABLE  SALTS  IN  THE  CORPUSCLE, 

Potassium  Sulphate 0. 132 

Potassium  Chloride 3. 679 

Potassium  Phosphate 2.343 

Sodium  Pliosphate 0.633 

Sodium  Carbonate 0. 341 

Calcium  Phosphate 0. 094 

Magnesium  Phosphate 0. 060 

PROBABLE  SALTS  IN  THE  PLASMA. 

Potassium  Sulphate 0.281 

Potassium  Chloride 0. 359 

Sodium  Chloride 5. 546 

Sodium  Phosphate 0. 271 

Sodium  Carbonate 1.532 

Calcium  Phosphate 0.298 

Magnesium  Phosphate 0. 218 

It  will  be  seen  that  the  corjjuscle  contains  an  excess  of 
potassium  salts,  and  the  plasma  contains  an  excess  of  sodium 
salts.     All  parts  of  the  blood  contain  salts,  however. 

Throughout  the  entire  body,  there  is  a  rich  supply  of  blood 
vessels  penetrating  every  tissue.  The  j^lasma  of  the  blood  j^ass- 
ing  l^y  exosmosis  through  the  walls  of  the  capillaries  is  thus 
brought  in  immediate  contact  with  the  tissues  to  which  it  brings 
nourishment  and  oxygen  of  the  blood,  and  from  which  it 
removes  the  waste  products  of  metabolism.  Other  usable  prod- 
ucts or  lymph  are  collected  in  small  capillary  spaces,  which  in 
turn  open  into  definite  lymphatic  vessels.     These  vessels  unite 


PKK'    ACID    AND    INTERSTITIAL    GINGIVITIS.  75' 

into  larger  and  larger  ones,  which  eventually  pour  this  usable 
waste  product  into  the  great  thoracic  or  left  lymphatic  ducts,  and 
a  second  smaller  right  lymphatic  duct.  These  in  turn  empty 
into  blood  vessels,  each  upon  its  own  side.  The  lymph  contains 
essentially  the  same  constituents  as  the  blood  plasma,  and  the 
salts  are  found  in  the  same  propoi'tion  as  in  it.  They  are  then 
eliminated  through  the  sweat  glands,  tonsils,  mucous  glands, 
kidneys,  large  intestines  and  salivary  glands. 

The  composition  of  the  deposits  in  the  various  parts  of  the 
body  vary  according  to  the  locality  and  the  character  of  the 
excreta  eliminated  in  connection  with  them. 

The  chemical  composition   of  the  human  bile,  according   to 
Jacobson,'  is  as  follows  : 

Water 977 .  40 

Sodium  Glycocholate 9 .  94 

Cholesterin 0.54 

Free  fat 0.10 

Sodium  palmitate  and  sterrate 1 .  26 

Lecitine ^ . .  . .  0 .  04 

Other  organic  matter 2 .  26 

Sodium  cliloride 5 .  45 

Potassium  chloride 0.28 

Sodium  phospliate 1 .  33 

Lime  pliosphate 0.37 

Sodium  carbonate 0 .  93 

Of  this  analysis  the  solid  ingredients  constitute  22.5  parts  per 
thousand,  of  which  two-thirds  .are  organic  and  one-third  inor- 
ganic. The  inorganic  salts  of  the  bile  are  in  most  cases  returned 
to  the  blood,  where  they  are  redistributed  to  the  tissues.  Occa- 
sionally, however,  gall  stones  occur,  which  are  composed  of 
(analysis  H.  D.  Geddings'-): 

Moisture 3 .  32 

Biliary  matter 32.182 

Cholesterin 54 .  952 

Matter  soluble  in   ether 7 .  77 

Iron traces 

Phosphoric  acid traces 

Lime traces 

Magnesiimi traces 

'American  System  of  Dentistry. 

-Transactions  South  Carolina  Medical  Association,  ISSO. 


76  IXTEESTITIAL    GINGIVITIS. 

SecKetions  of  the  pancreatic  juice  (dog)  by  C.  Schmidt  are  as 
follows : 

Water 900 .  76 

Solids 99.24       , 

Organic  substances 90 .  44 

Ash 8 .  80 

Sodium  carbonate 0 .  58 

Sodium  chloride 7.35 

Calcium  magnesium  and  sodium  phosphate 0 .  5.3 

■  The  comjiosition  of  the  normal  human  pancreatic  juice  has 
not  been  determined  comjjletely  owing  to  the  difficulty  of  obtain- 
ing the  secretion.  According  to  Zawadsky  the  composition  of 
the  secretion  of  a  young  woman  was  as  follows  : 

Water in  1.000  parts 864.05 

Organic  substance in  1,000  pai-ts 132.51 

Proteids in  1, 000  parts 92 .  05 

Salts in  1,000  parts 3  .  44 

INORGANIC   SALTS    IN    THE   SWEAT. 

"  Of  the  inorganic  salts,  NaCl  is  by  far  the  most  abundant ; 
it  occurs  in  quantities  varying  from  2  to  3.5  parts  per  thousand. 
The  elements  of  the  sweat  which  are  of  imjjortance  from  an 
excretory  standpoint  are  water,  inorganic  salts  and  urea  or  related 
nitrogenous  compounds. " 

Inorganic  salts  from  the  faeces  are  made  up  of  the  salts  of 
sodium,  jDotassium,  calcium,  magnesium  and  iron.  According  to 
Enderlin'  the  following  represent  the  composition  of  the  material 
matter  in  the  fseces  : 

SALTS    SOLUBLE    IN    WATER. 

Sodium  chloride  and  suljihate 1.37 

Sodium  phosphate 2 .  63 

SALTS    INSOLUBLE    IN    WATER. 

Earth  phosphate 80.37 

Ferric  phosphate 2 .  09 

Calcium  sulphate 4.53 

Silicic  acid 7 .  94 

Like  other  constituents  of  the  lymph,  the  salts  vary  consider- 
ably in  projDortion,  according  as  the  fluid  is  more  or  less  rich  in 

'  Gamgee,  Physiological  Chemistry  of  the  Animal  Body. 


URIC    ACID    AXD    INTERSTITIAL    GINGIVITIS.  77 

water.     The  salts  are  much  more  abundant  than    the  organic 
solids. 

Inorganic  salts  in  the  urine  consist,  according  to  Howell/ 
chiefly  of  chlorides,  phosphates  and  sulphates  of  the  alkalies  and 
the  alkaline  earths.  As  a  rule  they  arise  partly  from  the  salts 
ingested  with  the  food,  which  salts  are  eliminated  from  the  blood 
by  the  kidney  in  the  water  secretion,  and  in  part  they  are  formed 
in  the  destructive  metabolism  which  takes  place  in  the  body, 
particularly  that  involving  the  proteids.  Sodium  chloride  occurs 
in  the  largest  quantities  (about  15  grams  per  day),  of  which  the 
greater  j^art  is  derived  directly  from  the  salt  taken  in  the  food. 
The  phosphates  occur  in  combination  with  Ca  and  Mg,  but  chiefly 
as  acid  phosphates,  of  Na  or  K.  The  acid  reaction  of  the  urine 
is  caused  by  these  latter.  The  phosj^hates  are  produced  in  part 
from  destruction  of  phosphorus-containing  tissues  in  the  body, 
but  chiefly  proceed  from  phosphates  in  the  food.  Following  are 
the  average  quantities  in  grams  of  the  chief  substances  normally 
excreted  in  the  urine  in  six  hours  :' 

Water 1440      —  1500 

Solids , 57      —      68 

Organic  : 

Urea 28      —      68 

Uric  acid 7 

Hippuric  acid 3      —        2 

Kreatinin 1.7  —        2.1 

Inorganic  : 

Sodium  chloride 15      —      20 

Phosphoric  acid 2.5  —        3 

Sulphuric  acid 2      —        2.5 

Sodium 5      —        7 

Magnesium .04 

Potassium   3      —        4 

Calcium .03 

Urinary  calculi  (classified  according  to  their  principal  ingre- 
dients), are  divided  into  : 

1.  Uric  stone,  composed  of  uric  acid  and  acid  urates. 

2.  Oxalic  stone,  composed  of  lime  oxalate. 

3.  Phosphoric  stone,  which  are  composed  of  magnesium  phos- 
phate and  carbonate  with  urate  of  ammonia.  ' 

'  American  Text-Book  of  Physiolog}'. 
-  Landolt,  Ph\'siology. 


78  INTERSTITIAL    GINGIVITIS. 

Each  oue  of  these  compounds  is  nearly  in  a  j^ure  state.  A 
stone  may  be  composed  entirely  of  one  salt  or  it  may  be  comjiosed 
of  two,  three  or  four,  each  compound  forming  sej)arate  consecu- 
tive layers  through  the  stone.  One  examination  made  by  How- 
shij)  Dickinson'  showed  eighty-nine  per  cent  lime  carbonate  and 
the  rest  lime  oxalate  and  phosphate  of  lime. 

The  deposits  upon  the  teeth  are  derived  j^artly  from  the  salts 
ingested  with  foods,  which  salts  are  eliminated  from  the  blood  in 
water  secretion,  and  in  part  they  are  found  in  the  waste  of  tissue 
which  takes  place  in  the  body. 

The  saliva,  according  to  Schmidt,  is  made  up  of  the  following : 

Water 991 .  45 

Organic  material 2 .  89 

Inorganic  : 

Calcic  chloride 4.50 

Sodium  chloride .... 

Calcic  phosp)hate 1.16 

Magnesium .... 

1,000.00 

This  material  floating  in  the  saliva,  together  with  the  epithe- 
lial scales  and  other  extraneous  matters,  contribute  to  form  what 
is  known  as  tartar.  This  material  collects  ujaon  the  teeth,  and 
according  to  examinations  by  Stevenson  consists  of: 

Soft  tartar  Hard  tartar 

on  molars.         on  lower  incisors. 

Water  and  organic  matter 21 .  48      ....      17  .  51 

Magnesium  phosphate 1 .  31      ....        1.31 

Calcium  phosphate  with  a  little  car- 
bonate and  trace  of  fluorine....      77.21      ....      81.18 

100.00      ....    100.00 

Another  analysis  made  by  Scheheoetskey  resulted  thus : 

Water  and  organic  matter 22.  07 

Magnesium  j)hosphate 1 .  07 

Calcium  phosphate 67 .  18 

Calcium  carbonate 8.13 

Calcium  fluoride 1.55 

100.00 
'  Renal  and  Urinary  Afl'ections. 


URIC    ACID    AND    INTERSTITIAL    GIN(iIVITIS. 


79 


Malenfant  found  that  salivary  calculi  (located  in  Wharton's 
duct)  was  composed  of: 

Lime  jjhosphate 27 

Magnesium  phosf)hate 1 

Basic  lime  phosjDliate ....  60 

Alcohol  and  muriatic  acid 4 

Ptyalin 2 

Loss 6 

100 
The  following  are  results  of  analysis  of  salivary  calculi  by 
various  observers : 


Weight. 

100  Parts. 

Bivra. 

Lecanu. 

Besson. 

■1 

2 

3 

Bird. 

Calcium  carbonate.  .  . 

81.2 

79.4 

80.7 

13.9 

30 

15 

2 

Calcium  phosphate .  .  . 

4.1 

5.0 

4.2 

38  2 

75 

55 

75 

Magnesium  phosjahate 

5.1 

1 

Soluble  solids 

Organic    matter 

6.2 
7.1 

4.8 
8.5 

5.11 
8.3| 

38.1 

5 

25 

23 

Water  and  loss 

1.3 

2.3 

1.7 

6.3 

Deposits  in  the  tissues  in  gout  are  made  uj)  of  soda  and  lime 
urates.  In  order  to  compare  the  calcic  dejDosits  in  other  parts  of 
the  body  with  the  serumal  deposits  upon  the  teeth  affected  with 
interstitial  gingivitis,  thousands  of  teeth  were  obtained  from  three 
dental  offices  which  make  a  practice  of  extracting  teeth.  From 
these  one  thousand  were  selected  at  two  different  times,  making- 
two  thousand  teeth  containing  dejiosits  direct  from  the  tissues. 
These  were  submitted  to  a  chemical  analysis  by  J.  H.  Salis- 
bury, at  Rush  Medical  College,  who  reports  as  follows : 

"  The  method  which  I  employed  in  analysis  of  calcic  deposits 
was  as  follows :  The  material  was  so  selected  as  to  be  free  as 
possible  from  salivary  tartar  and  a  weighed  portion  was  dried  at 
100°  C  This  was  then  carefully  incinerated  and  again  weighed, 
and  the  iliflference  calculated  as  organic  matter.  The  residue 
after  incineration  was  divided  into  two  portions,  A  and  B. 

"A  was  used  for  the  estimation  of  phosphates  as  follows  : 
The  ash  was  dissolved  in  nitric  acid  and  the  solution  preci23itated 
with  ammonium  molybdate.  The  precipitate  was  washed,  dis- 
solved in    ammonia   precipitated   by  magnesia   mixture  and  the 


-80  INTERSTITIAL    GINGIVITIS. 

13recipitate  of  ammonia  magnesium  jjhospliate,  washed,  dried, 
ignited  and  weighed. 

"  In  B,  calcium  and  magnesium  were  estimated  as  follows  : 
The  ash  was  dissolved  iu  hydrochloric  acid  and  the  acid  just 
neutralized  with  ammonia  water  and  sodium  acetate  added.  It 
Tvas  then  made  slightly  acid  with  a  drop  of  hydrochloric  acid 
-and  precipitated  with  ammonium  oxalate.  The  precipitate  of 
calcium  oxalate  was  filtered  off,  washed,  converted  into  calcium 
•oxide  and  weighed.  The  filtrate  was  made  alkaline,  sodium 
jjhosjihate  added,  and  the  precipitate  of  magnesium-ammonium 
23hosphate  collected,  washed,  dried,  ignited  and  weighed.  In 
case  the  phos^^horic  acid  determined  in  A  did  not  saturate  the 
■calcium  and  magnesium  obtained  in  B,  the  excess  of  base  was 
calculated  as  carbonate. 

"The  following  is  the  comjDOsition  of  the  serumal  tartar 
according  to  analysis  of  April  18,  1898  : 

Water  and  organic  matter ' 32 .  24 

Magnesium  phosphate 98 

Calcium  phosphate 63 .  08 

Calcium  carbonate 3.70 

100.00 

"Analysis  of  the  serumal  tartar,  October  24, 1898,  shows  it  to 
iave  the  following  composition  : 

Water 4.48 

Organic  matter 27.00 

Calcium  phosphate 72 .  73 

Magnesium  phosphate 4.91 

99.12 

While  nearly  every  kind  of  food  taken  into  the  stomach  con- 
tains inorganic  salts,  every  excretory  organ  of  the  body  throws 
out  a  certain  amount  of  these  salts.  Some  of  these  organs 
excrete  the  salts  in  a  pure  state,  while  in  others  the  salts  are 
combined  with  acids  or  fluids  peculiar  to  that  organ.  These  salts 
differ  in  composition  and  quantity  on  different  days,  at  different 
hours  of  the  same  day  ;  differ  at  different  ages  of  the  same  person 
and  differ  in  jDcrsons  of  like  age,  on  the  same  diet.  No  matter 
how  careful  the  chemist  may  be  in  analysis,  no  two  results  will 
be  exactly  alike.     For  this  reason,  in  tartar  and  calcic  deposit 


URIC    ACID    AND    INTERSTITIAL    GINGIVITIS.  81 

upon  the  roots  of  teeth,  two  different  analyses  of  the  same  deposits 
are  cited.  It  is  evident  that  while  slight  differences  occur  in  the 
table,  these  are  due  chiefly  to  the  character  of  the  secretions. 
The  kidneys  and  salivary  glands  clearly  excrete  most  of  the  waste 
inorganic  salts. 

Since  each  excretory  organ  has  its  part  in  elimination  of 
waste  inorganic  salts,  it  is  clear  that  if  one  organ  becomes  tired 
or  diseased,  other  organs  have  an  extra  amount  of  material  to 
excrete.  In  any  event,  the  blood  becomes  surcharged  with  waste 
inorganic  salts.  There  is  a  class  of  patients  with  deformed  jaws 
and  irregular  teeth,  tonsil  hypertrophy,  mucous  membrane, 
nasal  bone  and  post-nasal  s^jace  disorder,  adenoids,  arrest  of  the 
facial  bones.  They  are  neurotics  and  degenerates.  This  class 
comprehends  those  whose  nervous  system  is  unstable  and  whose 
physical  development  is  a  departure  from  the  race  type.  This 
unstable  or  tired  condition  may  affect  but  one  excretory  organ. 
In  most  cases  it  affects  all  organs  as  well  as  the  entire  body.  In 
these  patients,  especially  in  youth,  does  hypertrop)hy  of  the  alve- 
olar process  take  place  and  large  deposits  are  observed  upon  the 
teeth.     In  this  class  may  be  placed  rachitic  children. 

Inorganic  salts  taken  in  food  are  generally  utilized  until  the 
osseous  system  has  attained  its  growth.  This  usually  occurs  at 
about  the  twenty-sixth  year,  but  full  growth  may  not  be  attained 
until  the  thirty-sixth  year.  When  this  period  has  been  reached, 
although  the  body  still  has  the  same  supply  of  inorganic  salts, 
the  system  can  assimilate  only  what  it  needs.  The  remainder 
becomes  waste.  Under  such  conditions  the  blood  is  overcharged 
with  these  salts. 

A  condition  of  the  system,  which  has  received  too  little  atten- 
tion, occurs  in  a  class  of  children  ranging  from  six  to  eight 
years,  who  excrete  larger  quantities  of  inorganic  salts  through 
the  kidneys  and  salivary  glands.  In  such  cases  the  teeth 
become  coated  with  tartar.  The  gums  become  inflamed  from 
irritation.  Interstitial  gingivitis  is  developed  in  youth.  These 
children  may  be  rachitic,  or  border  upon  the  disease.  They  are 
neurotic,  degenerate,  suffer  from  rachitis,  rapid  decay  of  the  teeth 
and  irregularities.  They  occur  in  American  and  European 
schools  of  idiocy  and  for  dependent  and  defective  children. 
From  seventy-five  to  ninety   per   cent  of  these  children    have 


82  INTERSTITIAL    GINGIVITIS. 

interstitial  gingivitis,  ranging  from  simple  inflammation  of  tli  e 
gums  to  absorption  of  the  gums  and  alveolar  process  with  pus 
exudate.  Miller  noticed  in  an  examination  of  twenty-six  cases 
of  rachitic  children  under  twelve  years  of  age  that  seven  mani- 
fested pronounced  symptoms  of  interstitial  gingivitis.  This  was 
no  doubt  due  to  accumulation  of  calcic  salts  upon  the  teeth, 
producing  irritation  and  absorption  of  the  alveolar  process  and 
contraction  of  the  gums. 

In  cases  where  large  collections  of  tartar  are  dej30sited  ui^on 
the  teeth  of  children  there  is  also  an  excess  of  excreta  through 
the  kidneys.  Examination  of  urine  in  such  cases  will  reveal 
always  from  four  to  eight  times  more  deposit  than  tlie  normal 
for  the  age  of  the  patient.  Defective  nutrition  is  the  result,  the 
bones  are  small,  and  the  jaws  and  teeth  are  irregular.  The  teeth 
decay  early  in  life  and  it  is  with  difficulty  that  the  decay  can  be 
arrested.  What  is  true  of  children  is  also  true  of  people  at 
advanced  age. 

■  After  the  skeleton  had  attained  its  growth  (even  in  those 
cases  where  no  deposits  were  before  observed)  the  blood  became 
overcharged  with  lime  salts  and  the  teeth  became  a  nidus  for  the 
deposit  from  the  salivary  glands.  It  is,  therefore,  clear  why 
deposits  and  inflammation  of  the  gums  are  so  common  after  the 
twenty-sixth  year,  and  more  common  later  in  life.  Defective 
children  and  people  who  have  obtained  their  growth  are  more 
susceptible  to  trojjhic  disorders  of  nutrition  and  the  tissues  take 
on  disease  more  readily  than  healthy  individuals  earlier  in  life. 
AVhen  inflammation  takes  place  in  connective  tissue  in  all  parts 
of  the  body  (especially  if  the  blood  be  surcharged  with  inorganic 
salts)  deposits  take  place  in  that  tissue  through  the  capillary 
system.  On  the  other  hand,  when  inflammation  of  the  connective 
tissue  takes  place,  if  inorganic  salts  be  scarce  in  the  blood, 
deposits  do  not  take  place.  As  is  elsewhere  shown,'  calcic 
dej)Osits  on  the  roots  of  teeth  are  a  result  of  inflammation  and 
pus  infection  and  not  the  cause. 

'  International  Dental  Journal,  April,  1896. 


CHAPTER   VII. 

HEREDITY    AND    ENVIRONMENT. 

The  influence  of  heredity  in  interstitial  gingivitis,  as  in  other 
morbid  conditions,  is  still  a  mooted  question.  Morbid  heredity, 
as  I  have  elsewhere  shown,'  is  practically  divisible  into  direct  and 
indirect.  In  the  first  type  the  morbid  condition  is  directly  inher- 
ited ;  in  the  second,  a  deficiency  is  due  to  the  morbid  condition 
which  may  or  may  not  express  itself  in  a  tendency  to  the  morbid 
condition  of  which  it  is  the  offshoot.  Heredity  further  should  be 
separated  from  congenital  states  which  result  from  the  operation 
of  germs  or  toxins  during  a  particular  pregnancy  wherein  these 
pass  through  the  j)lacenta  to  the  foetus.  A  child  may  l^e  Ijorn  of 
a  tuberculous  mother  with  a  tendency  to  tuberculosis,  but  the 
tubercle  bacili  may  also  directly  infect  it  through  the  placenta  so 
that  it  is  born  with  tuberculosis.  The  first  is  the  inheritance  of 
the  weakened  organism  of  the  mother.  The  second  is  a  condition 
of  intra-uterine  infection. 

The  reported  cases  of  direct  heredity  of  the  pyorrhoeic  stage 
of  interstitial  gingivitis  may  afford  instances  of  one  or  the  other  of 
these  categories.  As  has  elsewhere  been  shown,  transitory  organs 
are  peculiarly  apt  to  be  weakened  by  heredity  both  in  their 
structure  and  in  their  resistance  to  morbific  germs  and  agencies. 
These  weaknesses  are  especially  apt  to  l)e  shown  dui'ing  the 
period  of  systemic  stress  connected  with  the  first  and  second 
dentition.  Such  weaknesses  may  be  the  outcome  of  general 
nerve  exhaustion  on  the  part  of  the  parents  (the  mother  espe- 
cially),  and  constitutes  transformed  heredity,  which  is  far  more 
frequent  than  direct.  This  transformed  heredity  may  be  more 
intense  than  the  constitutional  deficiency  of  the  innnediate 
ancestry.  On  the  other  hand,  the  conservative  influence  of 
several  generations  may  so  oft'set  the  evil  results  of  the  defects  in 
the  parents  that  the  inheritance  of  defect  is  slight,  if  at  nil 
existent. 


'  Talbot :  Degeneracj' ;  Its  Signs,  Causes  and  Effects. 


84  INTEESTITIAL    GINGIVITIS. 

This  last  type  of  heredity  is  called  atavism  (or  "  throw-back,"' 
by  the  breeders).  It  is  more  likely  to  work  for  good  than  evil, 
albeit  the  evil  effects  are  more  generally  looked  for.  Because  of 
this  atavism  a  serious  nervous  defect  in  a  parent  might  express 
itself  only  in  an  increased  tendency  to  disease  on  the  jjart  of 
transitory  structures.  The  periods  of  stress  are  times  in  the  life 
of  man  when  certain  great  life  functions  are  developing  or  under- 
going retrogression.  These  periods  of  development  or  evolution 
are  marked  by  the  two  dentitions  and  the  development  of  the 
sexual  organs,  which  might  more  aptly  be  called  the  third  den- 
tition, since  ere  its  close  the  wisdom  tooth  appears,  if  at  all.  The 
periods  of  retrogression  are  when  the  great  sexual  functions  are 
undergoing  involution  or  when  the  whole  body  is  undergoing 
senile  change.  These  jj^i'iocl'^  often  constitute  an  etiologic 
moment  for  the  production  of  disease  even  when  potent  heredi- 
tary defect  is  absent,  albeit  at  these  periods  such  defect  is  apt 
to  ajDpear. 

Another  possibility  to  be  considered  in  this  connection  as 
complicating  the  diagnosis  of  heredity  in  disease  is  environ- 
ment, understanding  by  this  term  all  the  external  conditions  that 
can  favor  the  develojiment  of  a  disorder.  Family  habits  and 
surroundings  are  apt  to  be  alike  -for  every  member.  If  anything 
in  the  environment  especially  favors  the  breaking  out  of  a  disease 
in  one  member,  the  cause  is  equally  apt  to  be,  effective  with 
another,  provided  the  individual  idiosyncrasy  is  similar.  This 
may  give  rise  to  a  suspicion  of  heredity,  since  conditions  of  life, 
family  habits  and  intimate  household  surroundings  favor  the 
occurrence  of  a  disorder  in  several  members  or  generations  of  the 
same  family.  Habits  are  often  transmitted  by  imitation  from 
parents  to  offspring.  These  may  be  direct  exciting  or  predis- 
posing causes  of  an  affection,  especially  if  it  be  more  or  less 
favored  by  their  existence. 

That  constitutional  conditions  of  hereditary  origin  favor  the 
occurrence  of  interstitial  gingivitis  is  undeniable,  but  this  does 
not  prove  that  gingivitis  itself  is  hereditary.  They  favor  its 
occurrence  as  they  favor  other  morbid  conditions,  by  lessening 
resistance,  or  by  preparing  the  way.  The  gingivitis  is  only  one 
of  the  many  accidents  that  are  thus  facilitated.  So  far  as  sali- 
vary concretions  are  to  be  regarded  as  an  exciting  cause,  heredity 


HEREDITY    AND    ENVIROXMEXT.  85- 

may  be  disregarded,  since  these  (thougli  varying  widely  in  dif- 
ferent indivitluals  in  the  amount  of  the  deposit,  and  consequently 
the  irritation  produced)  are  dependent  upon  more  remote  con- 
stitutional or  local  conditions  without  direct  connection  with  the 
heredity. 

The  varieties  (charged  to  lithasmia  or  arthritic  conditions 
notoriously  hereditary)  are  of  accidental  origin  rather  than  essen- 
tially connected  with  constitutional  conditions  that  happen  to 
furnish  the  irritant. 

Local  uric  acid  jjoisoning '  is,  as  I  have  elsewhere  show^n, 
occasionally  associated  with  gingivitis.  The  coexistence  illus- 
trates the  lowered  vitality  of  the  system,  rather  than  the 
etiology. 

The  same  is  true  of  all  the  other  neurotic,  rachitic  and  degen- 
erative conditions,  hereditary  or  otherwise,  that  are  met  with, 
associated  with  gingival  inflammation.  They  all  favor  the 
occurrence  of  the  disease  by  causing  a  weakened  power  of  resist- 
ance predisposing  to  the  attack  of  any  irritation.  The  mouth, 
resistant  as  it  ordinarily  is,  is  at  all  times  open  to  irritation.  When 
resistance  is  impaired  it  gives  way  at  its  most  vulnerable  point, 
and  the  gingival  margin  is  one.  Interstitial  gingivitis  is  favored 
or  hindered,  like  other  disorders  of  its  kind,  by  constitutional 
conditions  which  may  or  may  not  be  inherited,  and  which  bear 
toward  it  the  relations  only  of  predisposing  and  accessory 
causes. 


'  Dental  Cosmos,  1896,  page  312. 


CHAPTER    VIII. 

DEGENERACY    AND    DEGENERATE    TISSUES. 

One  of  the  most  important  factors  of  predisposition  is  that  of 
degeneracy,  either  local  or  general.  Three  possibilities  of  life 
await,  as  has  been  elsewhere  pointed  out,^  each  living  being : 
either  it  remains  primitive  and  unchanged,  or  it  progresses 
toward  a  higher  type,  or  it  backslides  and  retrogresses.  The 
factors  underlying  the  stable  state  force  the  animal  to  remain  as 
it  is ;  these  underlying  the  progressive  tendency  make  it  more 
elaborate,  while  the  factors  of  degeneration  tend  to  simplify  its 
structure.  Degeneracy  is,  therefore,  a  gradual  change  of 
structure  by  which  the  organism  becomes  adapted  to  less  varied 
and  less  complex  conditions  of  life.  It  is  a  reverse  of  develop- 
ment which  proceeds  from  the  indefinite  and  homogeneous  to  the 
definite  and  heterogeneous  with  a  loss  of  explosive  force  diie  to 
the  acquirement  of  inhibitions  or  checks.  In  proportion  to  the 
depth  of  degeneracy  does  it  affect  the  earlier  simpler,  or  later 
complicated,  acquisitions.  The  opposite  process  of  progression  is 
a  gradual  change  of  structures  by  which  the  organism  becomes 
adapted  to  more  varied  and  more  complex  conditions  of  life.  In 
progression  there  is  a  new  expression  of  form  corresponding  to 
new  perfection  of  work  in  the  animal  machine.  In  degeneracy 
there  is  suppression  of  form  corresponding  to  the  cessation  of 
work.  Elaboration  of  some  one  organ  may  be  the  necessary 
accompaniment  of  degeneracy  in  all  the  others.  On  the  other 
hand,  degeneracy  in  one  organ  may  be  the  necessary  accomj)ani- 
ment  to  the  elaboration  in  all  the  other  organs.  During  the  period 
of  stress  defects  due  to  degeneracy  are  apt  to  appear  and  affect  the 
line  of  least  resistance,  determined  by  the  depth  of  degeneracy, 
as  well  as  the  variability  of  the  structures  concerned.  As  the 
teeth  and  jaws  are  among  the  most  variable  structures  in  the 
body,  they  are  peculiarly  apt  to  be  affected  by  either  general 
degeneracy,  which  affects  the  l^ody  as  a  whole,  and  has  local 

'  Talbot :  Degeneracy  ;  Its  Causes,  Signs,  and  Results. 


DEGENERACY    AND    DEGENERATE    TISSUES.  87 

expressions  or  local  degeneracy  by  wliicli  the  ]:)0(ly  l^enefits. 
The  foctors  jjroclucing  degeneracy  act  by  causing  nervous  exhaus- 
tion in  the  first  generation.  This  implies  a  practical  degenera- 
tion in  function,  since  tone  is  lost. 

Every  nerve  cell  has  two  functions ;  one  connected  with  sensa- 
tion or  motion,  and  the  other  with  growth.  If  the  cell  be  tired 
by  excessive  work  along  the  line  of  sensation  or  motion,  the  func- 
tion as  regards  growth  later  becomes  impaired.  The  cell  then 
not  only  ceases  to  continue  in  strength,  but  becomes  self- 
poisoned.  Each  of  the  organs  (heart,  liver,  kidneys,  etc.)  has 
its  own  system  of  nerves  (the  sympathetic  ganglia)  which,  while 
under  control  by  the  spinal  cord  and  brain,  act  independently. 
If  these  nerve  centers  become  tired,  the  organ  fails  to  perform  its 
functions,  the  general  system  becomes  both  poisoned  and  ill-fed, 
and  nervous  exhaustion  results.  In  most  cases,  however,  the 
brain  and  sijinal  cord  are  first  exhausted.  The  nerves  of  the 
organs  are  thus  allowed  too  free  play,  and  exhaust  themselves 
later.  This  systemic  exhaustion  has  local  expression  in  the 
testicle  in  the  male,  in  the  womb  and  ovaries  in  the  female. 
Through  this  the  body  is  imperfectly  supplied  with  natural 
tonics  (antitoxins)  formed  by  these  structures,  and  the  general 
nervous  exhaustion  becomes  still  more  complete.  All  the  organs 
of  the  body  are  weakened  in  their  function.  Practically  the 
neurasthenic  in  regard  to  his  organs  has  taken  on  a  degenerative 
function,  albeit  not  degenerating  in  structure,  since  the  rest- 
lessness of  the  organs  is  a  return  to  the  undue  expenditure  of 
force  which  occurs  in  the  lower  animals  in  proportion  as  it  is 
unchecked  by  a  central  nervous  system.  Through  the  influence 
of  various  exhaustion  agencies  the  spinal  cord  and  the  l>rain  lose 
the  gains  of  evolution  and  the  neurasthenic  is  no  longer  adjusted 
to  environment.  Since  the  reproductive  organs  suffer  partic- 
ularly, children,  born  after  the  acquirement  of  nervous  exhaus- 
tion, are  more  or  less  checked  in  development  as  the  influence  of 
atavism  is  healthy  or  not — have  degenerations  in  the  structure 
of  their  organs  which  in  the  parent  were  represented  Ijy  neuras- 
thenic disorder  in  function.  As  the  ovaries  of  the  neurasthenic 
woman  generally  exhibit  prominently  the  effects  of  the  nervous 
exhaustion,  the  offspring  of  these  do  not  retain  enough  vigor  to 
23ass  through  the  normal  process  of  develoimient. 


OO  INTERSTITIAL    GINGIVITIS. 

The  action  of  degeneracy,  considered  as  a  local  factor  of  con- 
stitntional  origin,  may  be  exerted  to  preserve  embryonic  con- 
ditions in  adult  life.  Such  preservation  may  result  in  the 
breakdown  of  tissues  which  would  otherwise  withstand  germs  or 
other  causes  of  disease  external  to  the  tissues.  Given  this  con- 
dition of  local  degeneracy,  a  local  predisj)Osing  factor  is  added 
to  both  the  exciting  causes  and  the  constitutional  predis]30sing 
factors.  So  long  as  the  teeth  and  transitory  structures  remain  in 
the  comparatively  stable  condition  of  primitive  races,  this  factor 
is  to  a  great  extent  in  abeyance.  When,  however,  the  jaw  begins 
to  evolve,  the  degenerate  types  find  this  factor  adding  dangers  to 
their  evolution.  In  the  degenerate  the  struggle  for  existence 
between  the  organs  is  not  properly  balanced,  whence  the  dangers 
from  these  local  states  of  degeneracy  that  in  the  higher  types 
are  expressions  of  advance  undergone  without  danger.  This  is 
excellently  illustrated  in  the  embryology  of  the  mucous  mem- 
brane. This  in  degenerate  children  often  fails  so  to  develop 
that  the  bactericidal  function  of  mucus  does  not  appear.  This 
hereditary  feebleness  of  the  mucous  membrane  is  j^eculiarly  apt 
to  occur  in  the  nose,  throat  and  gums,  but  other  mucous  mem- 
branes are  not  exemjjt. 


CHAPTER  IX. 

NEUROTIC,    DIATHETIC    AND    DEGENERATE    CHILDREN. 

Miller,  as  elsewhere  stated,  found  a  little  over  thirty-three 
and  one-third  per  cent  on  examination  of  twenty-six  rachitic 
children  under  twelve  years  who  manifested  interstitial  gingivitis. 
Considering  that  most  of  these  manifested  symptoms  of  inherited 
congenital  or  acquired  constitutional  defect,  such  a  small  propor- 
tion is  rather  remarkable.  The  fact  suggests  one  of  two  explana- 
tions —  either  the  children  in  the  institute  visited  by  Doctor 
Miller  took  better  care  of  their  teeth  and  gums  than  is  usual 
with  this  class,  or  the  cases  in  which  pus  existed  only  were 
classed  as  pyorrhoea.  I  have  examined  the  mouths  of  deaf- 
mutes,  blind,  idiotic,  feeble-minded  and  rachitic  children  in  the 
institutions  in  America  and  Europe.  Interstitial  gingivitis  was 
found  in  all  its  stages,  from  simjale  inflammation  of  the  gums  to 
loosening  of  the  teeth,  in  from  twenty-five  to  seventy-five  per 
cent.  In  these  cases  not  only  are  there  constitutional  factors, 
but  also  uncleanliness  of  the  mouth  and  gum  tissues.  The 
degenerate  children  encountered  in  office  jaractice  usually  have 
jaw  deformities  and  teeth  irregularities.  Patterson  has  had 
under  observation  thirty-eight  cases  of  well-marked  pyorrhoea, 
thirty-three  of  which  coexisted  with  nasal  catarrh.  These  cases 
were,  no  doubt,  those  of  degenerate  patients.  The  nasal  catarrh 
was  a  coincidence  dependent  on  the  general  deficiency  of  the 
mucous  membrane. 

Luxury  and  modern  degeneracy  are  generally  charged  with 
the  production  of  diseases  later  found  to  have  attacked  man 
in  prehistoric  periods.  This  has  been  the  case  with  interstitial 
gingivitis. 

R.  R.  Andrews  expresses  the  following  opinion  as  to  modes 
of  life :  "  I  have  been  led  to  believe  from  my  own  experience 
that  this  trouble  exists  largely  in  the  mouths  of  jieople  accus- 
tomed to  luxury  —  good  livers,  people  about  middle  age  who 
over-eat  and  under-work." 


90  IXTEE8TITIAL    GINGIVITIS. 

No  method  of  living  can  be  regarded  as  a  cause  of  this 
disease,  excej^t  so  far  as  it  affects  the  general  system,  thus  j^i'O- 
dueing  trojahic  changes.  There  is  probably  a  slight  difference 
in  liability  to  interstitial  gingivitis  between  ^^eople  of  sedentary 
habits  and  active  outdoor  workers,  as  well  as  between  animals 
domesticated  or  in  cai^tivity  and  those  which  run  at  large. 

It  is,  however,  obvious,  from  the  data  of  the  chapter  upon 
"  History,"  that  all  races  and  stations,  regardless  of  time,  climate, 
or  mode  of  life,  have  suffered  with  the  disease.  Examinations  of 
animals  in  the  American  and  European  zoological  gardens  show 
that  it  is  not  confined  to  any  class  of  animals.  Dogs  and  cats, 
wdiether  housed  or  I'unning  at  large,  suffer  with  it. 

The  question  how  far  this  region  is  affected  by  toxic  agents 
introduced  into  the  system  is  an  open  one ;  still  it  seems  probable 
that  they  exert  some  influence.  In  chronic  phosphorus  2>oison- 
ing  the  jaw  is  j)articularly  and  seriously  involved.  This  has 
laeen  attributed  chiefly  to  the  entrance  of  phosphorus  into  the 
deeper  tissues  through  carious  teeth  or  through  solutions  of  con- 
tinuity of  tissue  due  to  tartar. ,  In  the  case  of  other  poisons  this 
local  factor  is  not  so  evident.  Mercury  has  among  its  first 
effects  a  soreness  of  the  teeth  with  loosening  of  them  in  their 
sockets.  Here  it  appeai-s  that  the  alveolus  was  one  of  the  first 
special  points  of  attack  independent  of  any  traumatism  or 
abrasion  of  the  soft  tissues.  In  a  similar  way  the  toxins  of 
scurvy  directly  attack  the  alveolus.  Its  fleshy  covering  is  later 
involved  in  the  progress  of  the  disease.  This  sometimes  extends 
to  comjjlete  loosening  and  falling  out  of  the  teeth.  Here  an 
irritation  of  a  toxin  from  within  the  organism  has  a  point  of 
-election,  a  structure  that  from  its  constitution  or  other  reason  is 
particularly  vulnerable  to  attack.  Another  constitutional  dis- 
order in  which  the  alveolus  is  early  affected  is  diabetes.  The 
■exact  pathology  of  this  is  uncertain,  but  in  many  cases  at  least 
it  is  largely  dependent  on  disordered  action  of  the  central  nerve 
;system.  Renal  disease  is  another  common  condition  which  tests 
the  vulnerability  of  the  alveoli.  An  ideally  normal  kidney  is 
probably  rare,  but  only  when  its  abnormalities  pass  beyond  a 
certain  point  can  it  be  called  diseased.  In  the  less  advanced 
conditions  that  have  jDassed  the  line  of  morbidity,  alveolar  impli- 
cation is  often  very  marked.      This  may  l^e  one   cause  of  the 


NEUROTIC,    DIATHETIC    AND    DEGENERATE    CHILDREN.  91 

unusual  frequency  in  the  insane,  who  are  especially  liable  (as 
Bondurant '  and  others  have  shown)  to  suffer  from  renal  disease. 
They  are  very  liable  likewise  to  auto-intoxications  and  trophic 
disorders  as-  well,  since  the  balance  of  the  nervous  system  has 
been  disordered.  Some  (the  paretic  and  organic  dements) 
exhibit  especial  tendencies  to  trophoneurotic  disturbances  affect- 
ing the  teeth.  In  states  of  depression  and  stupor,  circulatory 
disturbances  predispose  to  these. 

The  constitutional  results  of  acute  and  chronic  infections  are 
apt  to  produce  auto-intoxication  in  addition  to  the  action  of  the 
toxins  of  their  germs.  The  eruptive  fevers,  especially  scarlatina, 
or  measles,  have  been  long  known  to  be  followed  by  wasting  or 
necrosis  of  the  alveoli.'  Here  the  condition  is  notably  symmet- 
rical and  unacconq^anied  by  exfoliation  or  necrosis  of  the  osseous 
system  elsewhere.  Tuberculosis  does  not  spare  the  alveolar  pro- 
cess. The  well-developed  disorder  known  as  Riggs's  disease  has 
been  charged  by  Robin  and  Magitot  to  the  direct  influence  of  the 
arthritic  (gouty  and  rheumatic)  process,  and  declared  a  special 
form  of  arthritic  manifestation. 

The  alveolus  is  clearly  vulnerable  to  the  toxins  of  many 
infectious  diseases.  It  is  also  quickly  affected  by  some  of  the 
autotoxic  influences  of  disordered  metabolism.  Its  vital  resist- 
ance to  these  agencies  is  less  than  that  of  other  tissues.  It  is  the 
earliest  sacrifice  when  these  toxins  or  all  toxins  disturb  the  har- 
mony of  the  organism. 

Another  cause  for  implication  of  these  parts  than  the  action 
of  toxins  exists.  Whenever  tissue  waste,  whether  local  or  gen- 
eral, exceeds  rej)air  there  is  trophic  change.  This  latter  depends 
directly  upon  disordei'ed  local  or  general  nervous  functions. 
Trophic  alterations  from  the  first  cause  appear  in  growth  disorders 
of  the  nails  and  loss  of  hair  (alopecia)  after  fevers — the  most 
familiar  obvious  examples  of  this  pathologic  process.  Of  the 
other  type  are  localized  neurotic  atrophies  where  the  direct  inter- 
vention of  toxins  can  be  excluded.  The  alveolus  is  liable  to  the 
first  form  of  trophic  deterioration.  The  influence  of  acute  dis- 
eases upon  the  alveolus  is  probabl}^  thus  exerted  in  many  cases 

'American  Journal  of  Insanity,  1892. 
-Kiernan,  Journal  of  Nervous  and  Mental  Diseases,  1878. 

"  Salter :  Transactions  of  Pathological  Society,  London,  18.59-60,  Vol.  X[,  page  309. 
Lucas,  Lancet,  1887,  page  692. 


92  INTERSTITIAL    GINGIVITIS. 

rather  than  by  direct  infection.  Where  no  cause  has  been  ascer- 
tained, examination  directed  to  this  factor  wouki  probably  reveal 
it.  The  general  failure  of  the  trophic  centers  after  the  prime  of 
life  (in  senile  states),  which  is  attended  with  loss  of  teeth  and 
wasting  of  the  alveoli,  is  perhaj)S  the  most  prominent  instance  of 
this  ty23e  of  trophic  failure  affecting  the  part.  Even  simple 
anaemia  may  thus  rise  to  alveolar  wasting. 

The  second  form  of  trophic  failure  in  the  alveolus  is  less 
prominent  siiice  it  generally  coexists  with  overshadowing  disturb- 
ance elsewhere  which  masks  it  to  a  certain  extent.  C  Cruveilier' 
noticed  its  occurrence  associated  with  paraplegia  and  invokes  a 
nervous  influence  in  its  causation.  In  facial  hemiatro23hy  local 
Ts^asting  of  the  alveolus  has  ap2oeared  before  the  disorder  had 
involved  generally  the  jaws.  This  may  sometimes  be  due  to  a 
local  cause,  but  its  occurrence  and  association  with  other  neviro- 
trophic  symptoms  is  suggestive. 

The  causes  which,  acting  locally,  produce  direct  interstitial 
gingivitis,  are  the  toxic  effects  of  mercury,  lead,  brass,  uric 
and  other  acids,  potass,  iodide,  and  other  agencies  acting  in  a 
similar  manner,  and  scurvy.  It  is  not  the  intention  to  enter  into 
an  elaborate  discussion  of  the  toxic  action  of  these  drugs,  but  in 
a  general  way  to  show  the  similarity  in  action  and  results  upon 
the  tissues.  Scurvy,  a  disturbance  of  metabolism,  produces  the 
same  train  of  symptoms  as  the  metals. 

It  is  a  widespread  opinion  among  dentists  that  in  toxic  cases 
the  gums  are  the  first  tissues  involved.  The  fact  is,  however, 
that  when  the  salts  of  mercury  are  taken  into  the  system,  as 
noted  elsewhere,  they  act  directly  upon  the  central  nervous 
system ;  later  occur  nausea  and  vomiting,  tremor  in  the  arms  and 
hands.  Besides  local  nerve  inflammation  (neurites),  mercurial 
and  brass  poisoning  jaroduces  j^aralysis  agitans,  and  lead  poison- 
ing, drop  wrist,  etc. 

Excessive  secretions  of  the  glands  of  the  body,  especially  the' 
salivary  glands,  later  occur  with  rise  in  temperature,  gingivitis 
with  periosteal  and  peridental  membrane  swelling,  thickening  of 
the  gums  and  loss  of  the  teeth.  The  central  nerve  system  dis- 
turbance affects  all  other  structures.  Inflammation  of  the 
mucous  membrane  of  the  mouth,  as  well  as  of  the  gums,  and  of 

'  Bilk.  Soc.  de  Chir.    Paris,  1870,  pages  30  and  31. 


NKUROTK',    DIATHETIC    AXD    DEGENERATE    CHILDllEX.  93 

the  alimentary  canal,  frequently  occurs  with  sloughing  of  tissue. 
The  kidneys  become  involved,  and  are  unable  to  carry  off  the 
eifete  matter. 

The  cachexia,  which  resembles  that  of  scurvy,  is  characterized 
by  great  debility,  anaemia,  emaciation,  aloi^ecia,  atrophy  and 
coarseness  of  the  nails,  with  pain  in  the  muscles  and  joints. 

]\Iercury  is  eliminated  by  all  excretory  organs  for  which  it 
has  a  great  affinity.  The  soluble  salts  pass  out  by  the  bowels. 
So  long  as  the  excretory  organs  of  the  body  eliminate  mercury, 
the  tissues  are  not  effected.  Small  closes  are  eliminated,  but  con- 
tinuation of  dosage  soon  involves  the  nervous  system,  and  after- 
w^ards  the  tissues  of  the  body,  esi^ecially  the  jaws.  The  first 
effect  of  mercury  upon  dogs  is  to  produce  vivacity  and  animation. 
This  lasts  for  two  or  three  days,  when  the  limbs  begin  to  trem- 
ble. The  kidneys  and  bowels  act  at  first  freely.  At  the  end  of 
seven  or  eight  days  paralysis  agitans  occurs.  There  is  constant 
trembling,  whether  when  awake  or  asleep ;  loss  of  appetite,  with 
slight  rise  of  temperature.  At  the  end  of  two  weeks,  the  gums 
become  inflamed  at  the  margins.  If  the  drug  be  continued, 
death  occurs  in  about  three  weeks.  The  loss  of  flesh  is  remark- 
able. Miners  working  in  mercury  mines,  and  looking-glass 
makers,  are  all  affected  to  a  greater  or  less  extent.  The  nervous 
system  is  always  involved.  The  kidneys  become  diseased.  The 
hair  drops  out.  The  miners  think  it  a  happy  issue  from  their 
trouble  when  they  have  lost  all  their  teeth,  or  even  the  molars. 
They  are  henceforth  exempt  from  suffering  so  far  as  the  teeth 
are  concerned.     Many  are  toothless  at  thirty-five. 

Mercury  taken  by  the  mouth  is  found  in  the  urine  in  two 
hours,  and  in  the  saliva  in  four  hours.  It  appears  in  the  urine 
fourteen  hours  after  it  has  been  applied  to  the  skin.'  Although 
it  is  believed  to  have  passed  entirely  out  of  the  system,  it  has 
been  found  in  the  brain,  liver,  kidneys  and  muscles.  It  is 
claimed  that,  like  lead,  it  forms  combinations  with  albuminoids 
in  the  tissues,  for  a  time  remaining  inert,  to  be  subsequently 
oxidized  and  returned  to  the  circulation  as  an  active  poison. 
While  a  single  dose  of  mercury  may  be  rapidly  eliminated  from 
the  system,  repeated  small  doses  distributed  over  a  long  period 
are  not  so  eliminated  on  account  of  the  thickness  and  occlusion 


'  Twentieth  Century  Practice  of  IMedicine,  Vol.  Ill,  page  935. 


94  INTERSTITIAL    C4INGIVITIS. 

of  the  walls  of  the  capillaries,  producing  endarteritis  ohliterans, 
hence  more  or  less  of  it  is  deposited  in  the  tissue. 

Lead  enters  the  system  through  the  alimentary  canal,  skin 
and  respiratory  tract.  A  longer  time  is  required  to  produce 
plumbism  (lead  poisoning)  than  mercurial  poisoning.  Lead  is 
stored  up  in  the  system  in  minutest  quantities  for  an  indefinite 
length  of  time.  Its  effects  are  not  manifest  until  the  central  and 
jDcripheral  nervous  systems  have  become  involved,  as  evinced 
by  the  effect  of  plumbism  upon  the  wrists.  Occasionally,  the 
chief  seat  of  deposit  is  the  liver  or  muscles.  It  is  chiefly  elim- 
inated through  the  kidneys,  and  very  slightly  through  the  liver 
and  salivary  glands.  Not  until  a  considerable  length  of  time 
has  elapsed  is  lead  traceable  upon  the  gums.  This  usually 
occurs  about  the  lower  incisors  and  cuspids.  This  deposit  (lead 
sulphite)  is  always  in  the  tissue  outside  of  the  blood  vessels. 
Plumbism  causes  trembling,  nausea  and  vomiting.  The  patient 
loses  flesh,  becomes  anaemic,  and  has  great  resultant  debility. 

The  lead  circulating  in  the  capillaries  accumulates,  owing  to 
imjDeded  circulation  resultant  on  a  thickening  of  the  coats  of  the 
vessel,  producing  occlusion.  A  bluish  line  upon  the  gums  indi- 
cates that  the  system  is  completely  saturated.  Like  mercury, 
lead  collects  in  the  mucous  membrane  upon  the  inside  of  the 
mouth,  producing  blue  patches  from  a  line  to  one-half  an  inch 
in  length.  Lead  not  only  produces  local  irritation,  but  affects 
the  peripheral  nerves  as  well,  producing  troj^hic  changes  ;  upon 
the  capillaries  a  thickening  of  the  inner  coat  results  in  endar- 
teritis obliterans.  Brass  j^roduces,  as  Hogben^  has  shown,  sim- 
ilar effects  to  mercury  and  lead ;  the  green  gum  is  an  early 
symptom. 

Potassium  iodide  exerts  a  like  toxic  influence  to  lead  and 
mercury,  as  its  pathology  is  similar  thereto,  but  it  is  of  infrequent 
occurrence. 

Scurvy  is  due  to  poor  food  and  hygiene.  Insufficient  alter- 
nation of  food,  impure  air,  want  of  bodily  exercise,  ennui  and 
uncleanliness  combine  the  causes  of  this  disease.  Previous  to 
the  introduction  of  canned  goods,  sailors  on  long  voyages,, 
prisoners  and  others  under  confinement  were  subject  to  scurvy. 
Lunatics,  idiots  or  j^eople  who  have  had  a  long  sickness,  are  now 

■  Birmingham  Medical  Review,  1887. 


NEUKOTK',  DIATHETIC  AND  DEGENERATE  CHILDREN.    95 

most  prone  to  it.  AntEinic  convalescents  from  protracted  fevers 
suffer  from  it. 

In  the  British  Arctic  Expedition  of  1875-76  over  forty-eight 
per  cent  of  the  men  suftereil  from  scurvy.  When  the  j^otato 
crop  failed  in  Ireland,  in  1846,  scurvy  became  prevalent.  In  the 
Crimean  war  23,000  cases  occurred  among  the  French  troops 
alone.  Scurvy  contributed  over  fifteen  per  cent  to  the  death  i-ate 
in  the  late  civil  war.     It  occurs  among  the  Klondyke  miners. 

In  public  institutions  for  degenerate  children  it  is  very 
prevalent.  I  have  observed  it  in  both  American  and  European 
institutions. 

Thomas  Barlow'  found  scurvy  associated  with  rachitis.  Sun- 
derland" found  that  rachitic  diathesis  was  a  very  strong  factor. 
Jacobi  reports  forty  cases  of  scurvy  and  rachitis.  Babies  in  good 
families  brought  up  solely  on  the  p)i"oprietary  infant  foods  are 
prone  to  scurvy.  They  lose  their  appetites,  become  pallid,  per- 
spire freely,  have  diarrhoea,  the  mouth  becomes  sore  with  inflamed 
mucous  membrane  and  gums.  Purpura  and  hfemorrhages  of 
mucous  membrane  are  common  with  pain  and  swelling  of  the 
joints. 

In  adults,  excess  of  sodium  chloride  in  the  blood  from  con- 
sumption of  salt  meats  and  fish  has  been  noted  with  scurvy. 
For  this  reason  Rawls,  of  Cincinnati,  Ohio,  believed  that  an 
excess  of  salt  in  the  system  produced  gingivitis.  Languor, 
depression,  anaemia,  with  a  rise  of  temperature,  and  enlarged 
joints  with  soreness  are  the  first  symjjtoms. 

The  effects  of  this  disease  upon  the  system  are  almost  identical 
with  those  of  mercury  and  lead.  Bruise-like  (purpuric)  erup- 
tions occur  upon  the  skin  and  mucous  membrane,  on  the  serous 
membrane  (notably  the  pleura,  pericardium,  meninges  and 
synovial  linings  of  the  joints),  mucous  membrane  of  the  mouth, 
stomach,  intestines  and  bronchi. 

Owing  to  the  ansemia,  vascular  weakness  and  altered  compo- 
sition of  the  blood,  oedema  is  connnon  both  in  the  lungs  and  in 
the  submucous  and  subcutaneous  tissue,  especially  the  feet  and 
legs.  The  gums  begin  to  swell  with  redness  and  fibrous  thicken- 
ing of  the  deeper  layer,  which  cause  protrusion,  especially  in 

1  Medical  Chir.  Trans.,  London,  Vol.  CXVI,  1883. 
-  Practitioner,  London,  February,  1894. 


96  INTERSTITIAL    GINGIVITIS. 

the  cases  of  degenerates.  The  blood  vessels,  especially  the  capil- 
laries, become  thickened,  in  some  cases  they  are  occluded,  or  ero- 
sion and  ulceration  occurs.  The  patient  becomes  decidedly  pale 
and  markedly  debilitated.  The  skin  is  dry  and  blanched.  Gen- 
eral emaciation  is  evident. 

The  mucous  membrane  and  gums  become  swollen  and  bleed, 
stomatitis  ulcerans  results  in  greater  or  lesser  degree.  The 
tongue  is  at  first  swollen,  then  it  becomes  dry  and  hard.  The 
gums  are  at  first  red  and  swollen.  They  bleed  easily  upon  the 
-slightest  touch.  Later  they  become  j^ale  and  are  irregularly 
larger,  somewhat  fungoid  and  friable,  protruding  between  the 
teeth.  They  are  quite  tender  to  the  touch.  Ulcers  appear  on 
the  buccal  surfaces.  The  stomach  becomes  irritable,  nausea  and 
vomiting  are  common.  Constipation  occurs  early  and  diarrhoea 
later  appears. 

Factors  acting  through  local  trophic  disturbances  are  not 
only  local  disorders  but  also  constitutional  diseases,  especially 
those  which  prevent  elimination  of  effete  matter  (Bright's  dis- 
•ease,  diabetes,  etc.)  skin  eruptions,  lung  affections,  auto-intoxica- 
tion (gout,  etc.)  and  conditions  like  pregnancy,  amenorrhoea, 
dysmenorrhea,  etc.  The  physiologic  processes  of  nutrition, 
growth  and  repair  are  regulated  by  local  nerves  which,  as 
already  pointed  out,  because  of  this  function  are  called  trophic. 
These  are  under  control  of  both  spinal  and  brain  centers.  Dis- 
orders of  the  local  nerve  or  of  the  higher  centers  may  produce 
trophic  change.  Such  disoi'ders  affect  more  decidedly  provi- 
sional structures,  since  the  growth,  nutrition  and  repair  of  these 
is  normally  unstable.  The  alveolar  process  is  an  outgrowth  of  a 
permanent  portion  of  the  skeletal  structure,  provoked  and  main- 
tained by  the  existence  of  what  are  really  dermal  appendages 
and  not  true  bones.  It  is  a  provisional  structure,  almost  unique 
of  its  kind  in  adult  life,  which  has  apjiarently  little  independent 
vitality.  This  is  in  part  due  to  mechanical  causes,  since  its 
.slender  structure  unsupported  by  the  teeth  offers  little  resistance 
to  impacts  from  without,  to  which  its  situation  renders  it  esi^e- 
cially  liable.  There  is  more  than  this  to  be  considered  in  reckon- 
ing the  special  vulnerability  of  the  alveolus.  It  is  protected  by 
a  thin  layer  of  fleshy  tissue  only,  which  itself  is  peculiarly  liable 
to  injuries,  thus  exposing  the  bone  to  infection.     There  is,  more- 


NEUROTIC,    DIATHETIC    AND    DEGENERATE    CHILDREN.  97 

over,  no  cavity  of  the  body  that  is  more  ojjen  to  germs  than  the 
mouth,  and  some  of  these  that  are  considered  especially  viru- 
lent are  its  constant  residents.  Access  of  germs  and  accidental 
pathogenic  factors  to  the  alveolus  is  constantly  afforded  by  cari- 
ous teeth,  the  irritation  of  tartar  deposits,  etc.  Its  liability  to 
disease  is  thus  indefinitely  increased.  As  it  is  not  very  resistant 
to  morbid  influences,  the  infections  have  thus  free  play,  hence 
supjxirative  disease  is  more  readily  induced. 

Great  practical  importance,  as  Hirt '  remarks,  must  be  attrib- 
uted to  the  changes  in  the  hair  and  teeth  which  are  observed  in 
tabetics  (locomotor  ataxia).  The  teeth  become  loosened  without 
pain  and  fall  out  without  appearance  of  inflammation ;  the  tooth 
being  seemingly  intact.  This  Hirt  ascribes  to  disturbance  in  the 
nutrition  of  the  jaw  ;  an  ati'ophic  change  connected  with  a  lesion 
of  the  nucleus  of  the  trigenimus.  The  fact  that  this  condition  is 
often  connected  with  laryngeal  crisis  tends,  in  Hirt's  opinion,  to 
support  the  view  of  Buzzard^  that  the  center  for  bone  nutrition 
lies  quite  close  to  the  vagus.  Similar  facts  have  been  observed 
by  C.  L.  Dana  in  America.  ^  The  conclusion  is  obvious  that  dis- 
turbance of  the  nerve  centers  governing  nutrition,  growth  and 
repair  exerts  the  same  influence  on  the  alveolus,  jaws  and  teeth 
as  similar  disturbances  do  upon  the  skin,  hair,  mucous  mem- 
branes and  bones  elsewhere. 

These  structures,  which  have  previously  become  affected  by 
disease,  although  the  patient  has  been  restored  to  health,  readily 
become  the  seat  of  interstitial  gingivitis.  This  is  illustrated  in 
those  persons  who  have  been  affected  with  scurvy,  salivation,  etc. 

'  Handbuch  der  Nerveiikrankheiten,  1896. 
-British  Medical  Journal,  February  19,  1886. 
^  Diseases  of  the  Nervous  System. 


CHAPTER  X. 

INTERSTITIAL  GINGIVITIS  IN  DOGS. 

The  technique  of  the  examinations  of  interstitial  gingivitis 
and  jjyorrhoea  alveolaris  in  dogs  was  as  follows  :  After  fixing 
and  hardening  in  two  per  cent  formalin,  alcohol,  or  Miiller's 
fluid,  the  tissues  were  decalcified  in  a  five  per  cent  alcoholic  solu- 
tion of  nitric  acid,  imbedded  in  celluloidin  and  stained  in  various- 
ways,  the  principal  ones  being  hfematoxylin  and  eosin.  Ten  or 
more  slides  would  be  obtained  from  each  tooth.  Out  of  these 
slides  have  been  selected  a  series  illustrating  the  progress  of  the 
disease  from  beginning  to  the  loosening  of  the  tooth. 

Fig.  31  is  a  longitudinal  section  of  a  cuspid  tooth  with  the 
alveolar  process  in  situ.  A  illustrates  the  enamel  of  the  tooth, 
(E)  the  ej)ithelium  passes  from  the  outer  margin  to  the  lower 
border,  then  folds  upon  itself  and  extends  down  the  side  of  the 
crown  of  the  tooth  as  far  as  the  neck.  Unfortunately,  in  this 
specimen,  the  structure  connecting  the  epithelium  and  the  fibrous 
tissue  of  the  periosteum  has  been  destroyed.  The  papillary  layer 
of  the  sub-epithelial  tissue  is  plainly  shown  at  the  outer  border. 
Small  round-cell  infiammation  may  be  seen  extending  along  the 
border  of  this  layer.  It  can  also  be  observed  extending  down 
the  capillary  blood  vessels  into  the  submucous  tissue  (SI  and  G). 

Fig.  32  shows  a  similar  section  of  another  tooth.  Here  the 
epithelial  structure  (E)  is  pulled  away  slightly  from  the  edge  of 
enamel  (A).  In  this  section  the  infolding  of  the  ejiithelium  is 
shown  at  the  neck  of  the  tooth.  This  structure  passes  downward, 
folds  outward  and  upon  itself  (AA)  and  returns  two-thirds  of 
the  distance  toward  the  gingival  border,  leaving  a  pocket  (RR). 
The  ejjithelium  (E)  is  very  dense  and  thick.  The  papillary 
layer  of  the  submucous  tissue  (G)  is  very  clearly  defined.  The 
capillaries  (K)  can  be  distinctly  traced  from  the  deeper  fibrous- 
tissue  through  the  submucous  layer  into  the  papillary  layer.  The 
thick  and  heavy  fibrous  tissue  of  the  periosteum  ("Dental  Liga- 
ment,"   Black)    may    be   seen    at    H,  inserted    firmly    into  the 


X  75.    A.  A.  obj.    Zeiss.    Micro-photog^raph,  reduced  one-third. 

Fig.  31.— Longitudinal  Section  op  Tooth  and  Glut  Tissue.    Slight  Gisgivitls.    Dog. 

A,    Enamel.        B,    Epithelial  Tissue.        G,    Submucous  Membrane.        M,    Fibrous  Tissue. 
SI,  Slight  Inflammation. 


X  75.    A.  A.  obj.    Zeiss.    Micro-photograpli,  reduced  one-third. 

Fig.  32.— Longitudinal  Section  of  Tooth  and  Gu.m  Ti.ssue.     Chronic  Interstitial 
Gingivitis.    Dog. 

A,  Enamel.  E,  Epithelial  Tissue.  G,  Submucous  Membrane.  H,  Periosteum. 
K,  Capillaries.  V,  Violent  Inflammation.  AA,  Point  of  Union  of  Epithelial  Tissue  and  Peri- 
dental Membrane.    ER,  Space  Pocket  from  want  of  Union  of  Epithelial  Fold. 


f 

h 

':^-  ' 

> 

«»' 

~ll 

w.-,,, 

% 

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**  . 

.      -v 

V 

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psfc  ■ 

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X  75.    A.  A.  obj.    Zeiss.    Micro-pholograph,  reduced  one-third. 

Fig.  33. — Longitudinal  Section  of  Alveolar  Process  and  Peridental  Membrane.    Slight' 
Interstitial  Gingivitis,  Extending  into  Alveol.ik  Process.    Dog. 

J,  Alveolar  Process.    L',  Inflammation  Extending  through  Enlarged  Haversian  Canals. 
■V,  Inflamed  Peridental  Membrane. 


X  75.    A.  A.  obj.    Zeiss.    Micro-photograph,  reduced  one-third. 

Fig.  34. — Longitudinal  Section  of  Alveolar  Proces.s  and  Peridental  Membrane.     Chronic 
Interstitial  Gingivitis,  Extending  into  Alveolar  Process.    Dog. 

H,  Periosteum.  J,  Alveolar  Process.  V,  Violent  Inflammation.  AA,  Point  of  Union  of 
Epithelial  Tissue  and  Peridental  IVIembrane.  I',  Inflamed  Peridental  Membrane.  L',  Inflam- 
mation Extending  through  Enlarged  Haversian  Canals. 


INTERSTITIAL    GINGIVITIS    IN    DOGS.  103 

ceiuentuiu  and  extending  outward  and  downward.  Just  below 
(A A)  may  be  seen  the  interlacing  of  the  coarser  fibers  of  the  peri- 
osteum with  the  finer  fibers  of  the  submucous  tissue.  Chronic 
i-ound-cell  infiammation  may  be  seen  extending  from  the  jiapil- 
lary  layer  through  the  capillaries  into  the  interstitial  tissue  of 
the  submucuous  layer  and  the  periosteum.  Marked  inflammation 
has  occurred  at  V.  The  openings  in  the  folds  of  the  epithelium 
are  fruitful  sources  for  the  accumulation  of  food,  epithelial  scales 
and  detritus,  in  which  fermentation  and  decomposition  from 
micro-organisms  result,  producing  inflammation. 

Fig.  33  is  a  section  through  the  peridental  membrane  (I)  and 
alveolar  process  (J)  at  the  lateral  incisor.  The  inflammation  has 
■extended  down  from  the  papillary  layer  through  the  submucous 
tissue,  the  fibrous  tissue  of  the  periosteum  into  the  peridental 
membrane  and  into  the  alveolar  process.  Round-cell  inflamma- 
tion may  be  seen  in  the  blood  vessels  extending  through  the 
Haversian  canals  (L^). 

Fig.  34  is  a  similar  section  from  another  tooth  showing  chronic 
inflammation  extending  throughout  the  jjeridental  membrane  (I) 
and  alveolar  process  (J).  The  Haversian  canals  (L)  are  well 
outlined  by  the  iiiflammatory  progress.  Marked  inflammation 
has  resulted  at  V  and  also  at  the  margin  of  the- alveolar  process. 

Fig.  35  is  a  section  of  the  ^jeridental  membrane  and  alveolar 
process,  illustrating  the  effect  of  interstitial  inflammation  upon 
the  blood  vessels  and  alveolar  process.  Chronic  inflammation 
•extends  throughout  the  peridental  membrane  with  very  decided 
inflammatory  change  (V).  The  cut  ends  of  the  blood  vessels 
which  were  originally  situated  in  the  Haversian  canals  are  seen 
(BV).  They  have  become  involved  with  the  result  of  a  thicken- 
ing of  the  walls  and  endarteritis  obliterans.  The  bone  about 
these  vessels  has  been  entirely  absorbed.  The  inflammation 
has  extended  beyond,  into  and  through  the  Haversian  canals, 
producing  the  type  of  absorption  of  the  trabeculiB  known  as 
halisteresis  ossium.  Lacunar  absorption  has  also  occurred  (O). 
Where  decided  inflammation  (V)  has  taken  place,  abscesses  are 
more  liable  to  occur  (as  will  be  noticed  later)  from  the  large 
number  of  blood  vessels  at  this  locality. 

Fig.  36  is  a  section  from  another  locati(jn  of  the  alveolar 
23rocess  witli  a  greater  amplification,  showing  the  inflanunatory 

8 


104  INTERSTITIAL    GINGIVITIS. 

process  extending  through  the  alveolar  process.  Endarteritis- 
obliterans  may  be  seen  in  different  localities  (EO).  Three  forms- 
of  absorption  are  evident  in  this  figure :  Enlarged  areas  arising 
from  absorption  of  the  trabeculse  (halisteresis  ossium)  due  to  the 
inflammatory  process.  The  vessels  of  Von  Ebner  precede  perfo- 
rating canal  absorption  (BB),  distributed  over  the  entire  field,  also 
the  result  of  the  inflammatory  j)rocess  and  lacunar  absorption  (O) 
which  may  result  from  inflammation.  As  long  as  the  fibrous  tissue 
remains  in  these  large  areas  to  retain  the  osteoblasts,  new  bone 
tissue  may  be  produced  under  favorable  conditions.  On  the 
other  hand,  when  this  tissue  and  the  osteoblasts  are  destroyed,  the 
alveolar  process  cannot  be  restored. 

Fig.  37  shows  a  section  of  the  alveolar  process  from  another 
dog.  Here  lacunar  and  other  absorption  (halisteresis  ossium)  are 
well  shown.  Thirty-seven  osteoclasts  (O)  may  be  counted  in  the 
field  while  destruction  of  bone  by  halisteresis  (Q)  is  rapidly 
going  on.  Remains  of  Haversian  canals  with  the  blood  vessels 
may  be  seen  (BV,  L).  In  the  discussion  of  the  peridental  mem- 
brane extending  into  the  alveolar  process  (page  37),  particular 
attention  was  called  to  the  fact  that  large  bundles  of  fibers 
extended  into  the  process  in  such  a  manner  as  almost  to  isolate 
portions  of  bone.  In  the  lower  left-hand  corner  (X)  may  be 
seen  two  pieces  of  the  alveolar  process  entirely  separated  from 
each  other  and  the  main  body  of  the  bone.  In  interstitial  gingi- 
vitis, it  is  not  uncommon  to  find  pieces  of  the  alveolar  process 
separated  by  halisteresis  and  lacunar  absorption.  When  loose 
teeth  are  extracted  as  a  result  of  this  disease,  pieces  of  the  alveolar 
process  come  away  with  the  peridental  membrane  attached  to  the 
tooth.  Fig.  66  was  obtained  in  this  manner.  In  the  upper  left- 
hand  corner  may  be  seen  eight  or  ten  new  osteoclasts  (O)  in  an 
enlarged  Haversian  canal,  at  work  isolating  one  piece  of  the 
alveolar  process  from  the  other. 

Fig.  38  shows  a  slide  from  still  another  dog.  Halisteresis  (Q) 
and  perforating  canal  (P)  absorption  are  here  well  shown.  In 
the  larger  space  at  the  lower  left-hand  corner  may  be  seen  two 
arteries  (EO)  which  were  originally  the  location  of  Haversian 
canals  and  which  have  thickened  walls  and  a  tendency  to  oblit- 
eration. The  light  color  shows  decalcification,  the  dark  normal 
bone.     At  P  may  be  seen  perforating  canal  absorption.     At  FGr 


A.  A.  oDj.     z,eiss.     Micrii-photOfii-aph,  reduced  one-third. 
Fig   35.- Longitudinal  Section  of  Tooth,  Alveolae  Process  and  Peridental  ME^tBRiNE 
Violent  Eound-Cell  Inflammation  of  Peridental  Membrane,  Extending  through  the 
Haversian  Canals  into  the  Alveolar  Process. 

C.Cementnm.  .T,- Alveolar  Process.  K,  Capillaries.  L,  Haversian  Cana]=;  NLar<.e 
Spaces  arising  from  Absorption  of  the  Trabecuhe,  starting  in  the  Haverskn  Canals  (HaliS 
MS).  O,  Lacunar  Absorption.  V,  Violent  Inflammation.  B V,  Blood  Vessels  ori-rinalh-  Havir 
EXiS^veSa^a^:^  ^^^'"^"*^^  ^^^■»'^---      ^■'   I"«a,nmation^.SS'\.l^^^^; 


X  150.    D.  D.  obj.    Zeiss.      Micro-photograph,  reauced  one-third. 
Fig   36.-LONGITUDINAL  Section  of  Alveolar  Process.    Chronic  Infla>>m..vtion  Extending 

THROUGHOUT,  SHOWING  H ALISTERE3IS,  PERFORATING  CaNAL  AND  LACUNAR  ABSORPTION.      DOG. 

J  Alveolar  Process  N,  Large  Spaces  arising  from  Absorption  of  the  TrabeculEe,  starting 
in  the  Haversian  Canals  (Halisteresis).  0,  Lacunar  Absorption.  P,  Perforating  Canal 
Absorption.  BB,  Blood  Vessels  of  V.  Ebner  preceding  Perforating  Canals.  EO,  Endarte- 
ritis Obliterans. 


X  75.    A.  A.  obj.    Zeiss.    Micro-photograph,  reduced  one-thirti. 
Fig.  37.— Longitudinal  Section  of  Alveolar  Process.    Chronic  iNFL.iM.M.iTioN  Extending 

THROUGHOUT,   SHOWING   HaLISTERESIS   AND    LACUNAR   ABSORPTION.      DoG. 

J,  Alveolar  Process.  L,  Haversian  Canals.  N,  Large  Spaces  arising  from  Absorption  of 
the  Trabeculs;,  starting  in  the  Haversian  Canals.  0,  Lacunar  Absorption.  Q,  Halisteresis 
Ossium  or  Decalcified  Bone.  X,  Remains  of  Calcified  Bone.  BV,  Blood  Vessels  originally 
Haversian  Canals. 


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X  75.    A.  A.  obj.    Zeiss.    Mioro-pliotograph,  reduced  one-third. 

Fig.  38. — Tean.svekse  Section,  Alveolae  Process.    Chronic  Inflammation  Extending 
throughout.    dog. 

J,  Alveolar  Process.  N,  Large  Spaces  arising  from  Absorption  of  the  Trabecute,  starting 
in  the  Haversian  Canals.  P,  Perforating  Canal  Absor]3tion.  Q,  Halisteresis  Ossium  or 
Decalcified  Bone.  X,  Remains  of  Calcified  Bones.  EO,  Endarteritis  Obliterans.  EG,  Fat 
Globules. 


X  rri.    A.  A.  obj.    Zeiss.    Jlicro-pholo^'i-aph.  reduced  ouelliird. 

Fig.  39. —  Cross  Section  of  Tooth,  Alveolae  Process  and  Peridental  BIembrane.     Chronic 
Inflammation  of  Peridental  Membrane  and  Absoriiion  of  the  Root  of  Tooth.    Dog. 

B,  Dentine.     C,  Cementum.     D,  Pulp.     I',  InHamed  Peridental  Membrane.      K,  Capillaries. 
S,  Root-absorptioD. 


X  75.    A.  A.  obj.    Zeiss.    Micro-photograph,  reduced  one-third. 
Fig.  40. —  Lokgitudin.-vl  Section  of  the  End  of  the  Root  of  a  Tooth,  Alveolar  Process 

AND   PeEIDENT.1L   MeMBEANE,    SHOWING   ClIRONIC  INFLAMMATION   OP  THE   PERIDENTAL  MeM- 

bkane.     Exostosis  of  the  Root  of  the  Tooth  and  Lacunae  Absorption.     Dog. 


C,  Cementum. 


D,  Pulp,  with  3  Foramina.      J,  Alveolar  Process.       O,  Lacunar  Absorption. 
P,  Perforating  Canal  Absorption.     CC,  Cementosis. 


X  75.    A.  A.  obj.    Zeiss.    Micro-photograph,  reduced  one-third. 

FiG.  41. — Cross  SEcrroN  op  Inflamed  Peridental  Membrane.     Dog. 

II,  Inflamed  Peridental  3Ienibi-ane.     W,  Epithelial  Debris. 


X  15.    75M.M.  obj.     Spencer.    Micro-photograph,  refluced  one-third. 

Fig.  42.  —  Longitudinal  Section  of  Tooth,  Alveolae  Process,  Peridental  Membrane, 
Showing  Interstitial  Gingivitis  and  Pyoerhcea  Alveolaris,  with  Tooth  Aboft  to  be 
Exfoliated.    Dog. 

C,  Cementum.  E,  Epithelial  Tissue.  H,  Periosteum.  I,  Peridental  Membrane. 
J,  Alveolar  Process.  K,  Capillaries.  L,  Haversian  Canals.  M,  Fibrous  Tissue.  R,  Pus 
Pockets.  U,  Nerve  Tissue.  V,  Violent  Inflammation.  AA,  Point  of  Union  of  Epithelial 
Tissue  and  Peridental  Membrane.    CC,  Cementosis.    DD,  Calcific  Deposits  Destroj^ed  bj'  Acids. 


X  40.    35  M.M.  obj.    Zeiss.    Micro-pliotogi'aph,  reduced  one-third. 

Fig.  43. — Longitudinal  Section  of  Tooth,  Alveolae  Process,  Peridental  Membrane  and 
Gum  Tissue,  Enlarged  from  Fig.  42,  Showing  Active  Inflajimation,  with  Pus  Pocket. 
Dog. 

C,  Cementum.  E,  Epithelial  Tissue.  G,  Submucous  Membrane.  I',  Inflamed  Peridental 
Membrane.  J,  Alveolar  Process.  L',  Inflammation  Extending  throush  Enlarged  Haversian 
Canals.  M',  Inflamed  Fibrous  Tissue.  R,  Pus  Pocket.  V,  Viorent  Inflammation.  AA,  Point 
of  Union  of  Epithelial  Tissue  and  Peridental  Membrane.  FF,  Food  Containing  Micro- 
organisms. 

113 


X  75.    A.  A.  obj.    Zeiss.    Micro-photograph,  reduced  one-third. 

Fig.  44. — Longitudinal  Section  of  Tooth,  Alveolar  Process,  Peridental  Membrane  anD' 
GoM  Tissue,  Enlarged  from  Fig.  42,  Showing  Active  Inflammation  with  Pus  Pocket.. 
Dog. 

C,  Cementum.      E,  Epithelial  Tissue.      J,  Alveolar  Process.      M',  Inflamed  FitooiLS  Tissue. 
R,  Pus  Pocket.     V,  Violent  Inflammation. 


INTERSTITIAL    GINGIVITIS    IN    DOGS.  115 

fat  globules  nui}^  be  seen,  while  in  the  larger  space  at  the  upper 
right-hand  corner  is  evident  entire  destruction  of  the  fibrous 
tissue. 

Fig.  39  illustrates  a  cross  section  of  alveolar  process  and 
cuspid  root,  showing  absorption  of  the  root.  Inflammation 
extends  throughout  the  peridental  membrane  (I).  The  cajDil- 
laries  (K)  are  quite  numerous.  These  are  cut  both  crosswise  and 
lengthwise.  Absorption  (S)  of  the  root  may  be  seen  progressing 
at  these  localities. 

Fig.  40  shows  a  longitudinal  section  of  the  end  of  the  root. 
Active  destruction  has  been  going  on  both  in  the  pulj)  chamber 
(D)  and  at  the  external  surface  of  the  cementum  (C).  The  irri- 
tation and  inflammation  has  caused  the  odontoblasts  to  fill  up  the 
pulp  chamber  with  secondary  dentine,  and  obliteration  of  the 
chamber  has  taken  place.  Below  the  constricted  j)ul2)  may  be 
seen  three  divisions  of  the  pulp  (D)  extending  through  three 
separate  canals  in  the  cementum  (C).  Cementosis  (CC)  may 
be  seen  at  the  end  of  the  root.  Lacunar  absorption  is  going  on 
(O).  Thus  results  a  building  up  and  tearing  down  of  the  same 
tissue  from  the  same  cause,  interstitial  gingivitis.. 

Fig.  41  shows  inflammation  of  the  peridental  membrane  (I') 
"with  epithelial  debris  (W)  scattered  throughout  the  field. 

Fig.  42  is  a  section  through  the  jaw  and  incisor  tooth,  showing 
the  relation  of  the  structures  to  each  other  in  a  severe  case  of 
interstitial  gingivitis  and  pyorrhoea  alveolaris.  The  tooth  is 
attached  at  only  a  very  small  portion  of  the  apical  end  of  the 
root.  The  disease  has  been  of  long  standing.  Absorption  of  the 
alveolar  process  on  one  side  has  progressed  on  fully  one-half  of  the 
root,  while  upon  the  other  about  one-third  the  distance.  Inflam- 
mation commenced  at  the  gingival  boi'der  and  extended  through 
the  periosteum  (H),  peridental  membrane  (I)  and  alveolar 
process  (J).  Marked  inflammation  (V)  has  occurred  in  the 
mucous  membrane  fold.  An  abscess  has  formed  with  a  fistula 
extending  to  the  gingival  border.  The  thin  border  at  the  left  of 
the  fistulous  tract  is  the  epithelium  layer  next  to  the  tooth.  It  is 
evident  that  the  pus  burrowed  to  the  snrfice  through  the  struc- 
ture instead  of  between  the  epithelium  and  the  tooth.  A  similar 
abscess  and  fistulous  tract  are  evident  upon  the  gingival  border 
on  the  opposite  side  of  the  tooth.     The  irritation   produced  bv 


116  INTERSTITIAL    GIXGIVITIS. 

the  movement  of  the  tooth  has  caused  the  cementoblasts  to 
deposit  large  quantities  of  material  upon  the  sides  and  the  end  of 
the  root.  The  main  nei've  trunks  (U)  may  be  seen  at  and  below 
the  end  of  the  root. 

Fig.  43  illustrates  the  alveolar  border  on  the  right  side  of 
Fig.  40,  greatly  amplified.  This  shows  the  progress  of  intersti- 
tial gingivitis  extending  through  the  alveolar  process  producing 
absorption  with  intense  inflammation  of  the  peridental  membrane 
and  abscess  with  fistulous  tract. 

Fig.  44  shows  a  similar  process  amplified  from  the  left  side  of 
Fig.  42.  It  is  interesting  to  note  in  this  illustration  that  the 
fibers  of  the  sub-epithelium  pass  down  and  become  interwoven 
with  the  coarser  fibers  of  the  periosteum  in  just  the  023j)Osite 
direction  from  those  in  the  other  side  of  the  tooth,  and  in  other 
illustrations.  The  fibers  from  the  mucous  membrane  along  the 
side  of  the  tooth  extend  down  and  into  the  peridental  membrane, 
without  a  break  in  the  structure.  The  arrangement  of  the  fibers 
of  the  submucous  layer  in  producing  the  fold  is  well  illustrated 
in  the  figure.  This  picture  illustrates  inflammation  starting  in 
the  o'ingival  border. 


CHAPTER  XI. 

MERCURIAL    INTERSTITIAL    GINC4IVITIS    IN    DOGS. 

To  secure  a  chain  of  evidence  that  interstitial  gingivitis  (due 
to  the  metals,  drugs,  uric,  lactic  and  other  acids)  commenced  in 
the  papillary  layer  of  the  sub-ej^ithelial,  mucous  membrane,  I 
instituted  a  series  of  experiments  in  mercurialization   of  dogs. 


Proj.  14  inch,  ocular  lii  inch.    Spencer. 

Fig.  4.5. — Longitudinal  Section  op  Gingival  Boedke,  Showing  Eound-Cell 
Inflajimation  Due  to  Mercurial  Poisoning. 

Dogs  for  the  purpose  were  picked  up  in  the  streets.  Some 
of  these  were  operated  upon  by  myself,  but  most  of  them  were 
under  treatment  at  the  Post-Graduate  Medical  School.  Care 
Avas  taken  to  secure  those  in  health  and  with  healthy  gums. 
Mercury   was  introduced   l)y  the   mouth,  skin   and   liypodermic 


118 


INTERSTITIAL    GINGIVITIS. 


injection.  It  was  no  easy  matter  to  get  them  under  influence 
of  the  drug,  since  the  power  of  the  glands  to  elimina,te  the  poison 
was  enormous.  In  no  case  was  salivation  produced.  The  first 
symptom  noticed  was  exhilaration,  which  would  last  from  three 
days  to  a  week.  Then  paralysis  agitans  would  continue  until 
death.  In  about  a  week  the  appetite  would  commence  to  fail 
and  it  was  difficult  to  get  the  dogs  to  take  food  of  any  kind. 
The  kidneys  and  bowels  eliminated  the  poison.     There  was  a 


Pantachr.  oil  imm.  iV  inch  ocular.    No.  3.    Leitz. 

Fig.  46. — Longitudinal  Section  of   Gingival  Border.       Higher  Magnification, 
Showing  Connective  Tissue  Infiltration  with   Plasma  Cells  and  Polynu- 

CLEAR   LeUCOSYTES.      DoG. 

rise  in  temperature.  Some  of  the  dogs  died  before  gingivitis 
was  observed.  This  demonstrated  that  not  only  does  the  nervous 
.system  become  involved,  but  the  organs  of  the  body  may  be 
morbidly  affected  and  death  ensue  before  the  gums  show  symp- 
toms of  disease.  Some  dogs  were  killed  after  the  gums  became 
diseased.  The  time  required  to  obtain  results  was  from  three  to 
eight  weeks.     The  age  and  physical  condition  of  the  dog  caused 


MERCURIAL    INTERSTITIAL    GINGIVITIS    IN    DOGS. 


119 


this  variation  in  time.  After  death  the  gum  tissue  was  dissected 
from  different  parts  of  the  jaws  and  phxced  in  either  fifty  per 
cent  alcohol,  Miiller's  fluid,  or  two  per  cent  formalin. 

Sections  of  tissue  from  the  gum  margin  and  sides  were  made 
on  a  number  of  places.  Some  were  imbedded  in  paraffin,  others 
in  celluloidin.  The  sections  were  stained  according  to  various 
methods :  Delafield's  hsematoxylin,  eosin  (Unna's),  alkalin 
methylblue,  carmin,  Gramm's  stain,  etc. 


Fantaclir.  oil  imm.  i\  inch  ocular.    No.  :i.     Leitz. 

Fig.  47. — Longitudinal  Section  of  Gingivat,  Boedek.  Higher  Magnification, 
Showing  Round-Cell  Inflammation  Extending  to  the  Inner  Coat  of  the 
Blood  Vessel  and  also  Plasma-mast  Cells. 


Microscopic  examination  showed  that  the  epithelial  lining  of 
the  gums  did  not  present  pathologic  changes,  but  appeared 
normal  in  every  respect.  Connective  tissue  below  the  gum 
epithelium  (the  tissue  analogous  to  the  papillary  layer  of  the 
derma  and  the  derma  proper)  presented  unmistakable  evidences 
of  a  mild  inflammatory  process.  There  occurred  in  this  con- 
nective tissue  round-cell  infiltration,  oenerallv  moderate  l)ut  in 


120 


INTERSTITIAL    GINGIVITIS. 


some  places  quite  dense.  This  cellular  infiltration  extended 
from  below  (where  it  was  densest)  upward  into  the  papillary 
layer  (Figs.  45  and  46).  The  densest  cellular  infiltration 
usually  occurred  around  the  vessels  (Fig.  46). 

Under  high  magnification,  the  cellular  infiltration  was  found 
to  consist  of  polymorphonuclear   leucocytes,  plasma  cells    and 


Projection  %  inch,  ocular  1'/^  incli.    Spencer. 

Fig.  48. — Longitudinal  Section  or  Gingival  Boeder,  Showing  Round-Cell  Infil- 
tration IN  the  Connective  Tissue  and  Extending  into  the  Papill.e.    Dog. 


plasma-mast  cells,  the  latter  with  coarse  basophilic  granulations 
(Figs.  47  and  48). 

In  some  places  were  seen  between  the  round  cells,  short, 
broad  fusiform  cells,  the  protoplasm  of  which  took  quite  well 
basic  methylblue.  These  cells  resemble  very  much  fibroblasts 
and  appear  to  be  derivations  of  the  plasma  cells  (Fig.  49).  No 
bacteria  were  found  either  in  the  areas  of  cellular  infiltration 
(inflammatory  areas)  or  elsewhere.  In  these  cases  it  is  obvious 
that  there  had  occurred  a  mild  inflammation  of  the  gums  (gingi- 


MERCURIAL    INTERSTITIAL    GINGIVITIS    IN    DOGS. 


121 


vitis).  While  this  couhl  not  be  seen  with  the  naked  eye, 
microscopic  examination  demonstrated  histologic  features  of  an 
inflammatoiy  process.  The  absence  of  bacteria  justified  the 
belief  that  this  inflammation  was  not  of  microbic  origin,  but  due 
to  mercury,  which  by  its  well-known  chemotactic  influence  pro- 
duced the  histolos'ic  changes  of  an  inflammation. 


Pantachr.  oil  imm. 


iich  ocular.    No. 


Fig.  49. — LoxtiiTUDiNAL  Section  of  Gingival  Border,  Showinu  Round-Cell. 
Inflam.mation  Due  to  Mercurial  Poi.soninci.     Higher  MAcisiFicATiON. 


CHAPTER  XII. 

BACTERIOLOGY    OF    INTERSTITIAL    GINGIVITIS. 

The  bacteric  etiology  of  interstitial  gingivitis  has  been  inci- 
dentally discnssed  by  many  wi'iters. 

Gali2325e'  was  probably  among  the  first  to  make  analytic 
experimentation  in  the  bacteriology  of  this  disease.  He  claims 
that  there  is  found  in  the  pus  of  pyorrhoea  a  parasite,  resembling 
in  shape  the  Greek  letter  N.  Injecting  this  into  the  belly  of  a 
guinea  j)ig,  abscesses  resulted,  which  had  a  special  tendency  to 
affect  bone  tissue.  Injections  into  the  space  between  the  teeth 
and  gums  were  negative  in  result.  Galippe  regards  his  experi- 
ments as  suggestions  for  further  research,  but  not  demonstra- 
tive. Miller,"  after  explaining  his  own  methods,  made  a  series  of 
'Culture  experiments  on  agar-agar  at  blood  temperature.  Twelve 
cases  of  pyorrhoea  in  human  beings,  and  six  in  dogs,  were  exam- 
ined. He  isolated  twenty  different  bacteria  from  human  beings, 
and  nine  from  dogs.  Among  the  twenty  kinds,  staphylococcus 
pyogenes  aureus  was  found  twice.  Staj)hylococcus  pyogenes 
albus  once,  streptococcus  pyogenes  once.  Of  the  other  sixteen, 
nine  subcutaneously  injected  produced  no  particular  reaction, 
four  a  slight,  three  a  severe  suppuration  in  the  subcutaneous  con- 
nective tissue Among   the  nine  species  found  in 

dogs,  staj)hylococcus  pyogenes  albus  occurred  once.  Of  the 
-other  eight,  two  subcutaneously  injected  caused  no  reaction,  and 
five  but  slight.     One  caused  very  profuse  sujjpuration,  by  which 

large  portions  of  skin  exfoliated Microscopic  exami- 

jnation  of  stained  sections  revealed  masses  of  different  bacteria, 
-cocci  and  bacilli.  Leptothrix  occurred  infrequently,  and  then 
'Only  on  the  surface  of  the  cement,  and  where  there  were  micro- 
scopical cavities  in  it Miller  succeeded  consequently 

in  cultivating  a  large  number  of  bacteria  from  pyorrhoea  alveo- 
laris  which  possessed  jjyogenic  properties,  but  was  not  able  to 

'  Die  Infectiose  Arthro-Dentiiire  Gingivitis,  1888. 
^  Micro-Organisms  of  the  Human  Mouth. 


BACTERIOLOGY    OF    INTERSTITIAL    GINGIVITIS.  VIS- 

determine  the  constant  occurrence  of  any  one  which  might  be 
regarded  as  the  si^ecific  micro-organism  of  pyorrhcea  alveolaris. 
jNIiller  remarks  that  it  is  not  evident  from  Galippe's  communica- 
tion whether  he  found  the  N  or  ,3  bacterium  in  all  cases  exam- 
ined, or  but  once. 

Sudduth,  after  repeated  examinations,  arrived  at  the  same 
conclusion  as  INIiller. 

The  results  obtained  in  the  Columbus  INIemorial  Laboratory 
of  Chicago,  by  W.  A.  Evans,  Avere  as  follows : 

In  order  to  determine  wdiether  a  specific  bacterium  existed  in 
the  pyorrhoeic  stage  of  interstitial  gingivitis  in  man  (necessary 
to  constitute  this  stage  a  special  disease),  pus  from  more  than  fifty 
cases  was  examined.  In  all,  the  pus  was  obtained  from  the  gums 
by  a  platinum  needle  under  proper  methods  of  sterilization.  The 
pus  from  some  cases  was  smeared  on  a  slide.  This  was  stained 
and  such  determination  made  as  was  possible  with  this  proce- 
dure. With  the  pus  from  fifteen  cases,  agar  was  inoculated  and 
placed  in  Petrie's  dishes.  The  individual  colonies  were  grown 
on  gelatin,  agar,  bouillon,  potato  and  blood  serum.  The  results 
were  as  follows :  In  fifteen  cases  in  which  the  organisms  were 
plated  out,  fifty-five  organisms  were  found.  In  two  there  was 
no  growth.  Two  had  but  one  species  of  germs,  two  had  six,  one 
had  seven,  and  one  had  ten.  The  germs  found  are  divisible  into 
three  classes :  Those  usually  pathogenic  to  man,  those  excep- 
tionally 23athogenic  to  man,  and  those  never  pathogenic  to  man. 
The  first  class  was  found  thirty  times,  the  second  twelve,  and  the 
tliird  thirteen.  Class  third  is,  no  doubt,  seemingly  smaller  than 
it  sh(juld  be,  since  many  members  of  it  probably  do  not  grow  on 
ordinary  culture  media.  Of  the  germs  most  frequent  and 
important,  staphylococcus  pyogenes  aureus  occurred  nine  times, 
staphylococcus  pyogenes  albus  six  times,  and  staphylococcus 
pyogenes  citreus  once.  A  lanceolate  diplococcus,  growing  like 
pneumonococcus,  was  found  six  times.  Streptococcus  pj^ogenes 
was  found  twice.  Bacillus  coli  commune  w^as  found  twice.  A 
bacillus  growing  like  the  diphtheria  bacillus  occurred  twice. 
This  last  bacillus  had  the  appearance  of  the  Kleb-Loeffler  bacil- 
lus. It  lay  on  the  slide  like  it  and  it  stained  irregularly.  Of 
the  less  important  organisms,  bacillus  jjyocyaneus  was  found  thi-ee 
times,  micrococcus  tetragenus  seven  times,  leptothrix  seven  times. 


124  INTERSTITIAL    GINGIVITIS. 

bacillus  meseutericus  twice,  bacillus  subtilis  three  times.  There 
was  also  j)i'esent  a  peculiar  large  club-shaped  fungus  somewhat 
resembling  the  degenerative  forms  of  actinomycosis. 

Did  these  examinations  stand  alone,  definite  conclusions  could 
not  be  drawn  from  them.  These,  however,  are  admissible  since 
all  observations  on  this  subject  tend  in  the  same  direction. 
"While,  as  already  stated,  Galipj^e  believed  that  he  had  isolated 
two  bacteria  capable  of  causing  pyorrhoea  alveolaris,  still  he 
failed  with  both  to  produce  the  disease.  This  failure,  according 
to  the  laws  of  Koch,  is  fatal  to  the  position  taken. 

M.  Herzog,  of  the  Chicago  Polyclinic,  on  examination  of 
cases  of  iutei'stitial  gingivitis,  which  had  not  reached  the  i^yor- 
rhoeic  stage,  had  the  following  results  :  Pieces  from  the  gum  mar- 
gin which  had  been  fixed  and  hardened  in  a  formalin  solution, 
were  partly  imbedded  in  celloidin,  jmrtly  in  paraffin.  The  sec- 
tions were  stained  according  to  various  methods,  including 
Gramm's,  eosin  (Unna's)  and  alkaline  methylblue  stain.  The 
examination  of  the  tissue  shows  an  unchanged  lining  of  stratified 
squamous  epithelium,  and,  in  the  connective  tissue  below  the 
former,  well-marked  evidences  of  an  inflammatory  process.  The 
round-cell  infiltration  is  best  marked  in  the  deeper  layers  toward 
the  23eriosteum,  while  the  layers  of  connective  tissue  fibers  nearer 
to  the  lining  epithelium  show  less  evidences  of  inflammation  and 
are  partly  entirely  free  from  any  round-cell  infiltration.  The 
infiltrating  round  cells  are  of  the  type  of  lym2:)hocytes,  plasma 
cells  and  plasma  mast  cells.  Very  large  and  typical  mast  cells 
are  frequently  found  in  the  neighborhood  of  small  vessels. 
Many  of  the  vessels  seen  are  quite  tortuous,  and  the  vascular  sup- 
ply of  the  connective  tissue  apj^ears  to  be  considerably  increased 
beyond  the  normal.  Bacteria  could  not  be  demonstrated  in  the 
inflamed  areas. 

M.  Herzog's  examination  of  the  interstitial  gingivitis,  pro- 
duced by  mercury  in  dogs,  failed  to  reveal  any  bacteria.  He  was 
of  opinion  that  the  histologic  changes  of  inflammatory  tyjje 
found,  were  due  to  the  chemotactic  influence  of  mercury  and  not 
to  microbic  action. 

In  a  paper'  read  before  the  Section  on  Stomatology  of  the 

'  Some  Points  on  the  Etiology,  Pathology  and  Treatment  of  Pereistent  Pyorrhoea 
Alveolaris. 


BACTERIOLOGY    OF    INTERSTITIAL    GINGIVITIS.  125 

American  IMedical  Association,  at  Columbus,  Ohio,  George  T. 
Carpenter  mentioned  some  very  interesting  experiments  in  this 
connection.  By  infecting  a  fresh  wound  in  the  gums  of  rabbits 
with  pyorrhoea  and  other  ^his  he  found  the  parts  will  remain 
infected  only  from  two  to  five  days.  In  other  rabbits  a  rubber 
band  was  placed  around  teeth  and  pressed  under  the  gums  until 
inflammation  resulted,  when  the  parts  were  infected  with  pyor- 
rhrea  and  pus  from  a  chronic  ulcer ;  j)us  infection  resulted. 

Like  experiments  were  made  in  the  human  mouth  on  gums 
which  had  been  neglected  as  well  as  on  healthy  gums,  and  with 
similar  results.  His  experiments  tend  to  show  that,  when  animals 
and  man  are  healthy,  the  tissues  resist  infection ;  but  when 
diseased,  infection  results.     All  yield  to  treatment. 

On  examination  of  pus  taken  from  pyorrhoea,  pockets  ])yo- 
ceeding  from  acute  infection,  two  competent  bacteriologists  were 
unable  to  find  a  micro-organism  not  found  in  pus  from  other 
infected  tissues. 

These  results,  in  Carpenter's  opinion,  tend  to  show  that  a 
specific  germ,  to  which  pyorrhoea  alveolaris  is  attributable,  has 
not  yet  been  found. 

The  disease  being  so  prevalent  among  dogs,  it  occurred  to  me 
that  they  would  be  of  great  value  for  exjjerimental  inoculation. 
The  jsrevalence  of  the  disease  in  dogs  suggests  that  if  it  were  a 
specific  infection,  these  must  be  inoculable.  Miller'  had  made  a 
few  inoculations  of  pus  as  well  as  of  the  deposits  around  the 
teeth.  81ight  inflammation,  and,  in  one  case,  a  little  supjjuratiou 
alone  resulted.  He  afterward  isolated  twenty  different  bacteria 
from  the  human  mouth  and  nine  from  dogs.  Some  of  the 
uncommon  varieties  were  infective,  but  without  marked  results. 
Isolated  varieties  would  probably  not  produce  results  that  could 
be  attained  by  inoculating  animals  with  the  fresh  secretion  (j^us 
and  other  deposits)  from  dogs  already  affected  with  the  disease.  A 
dog  was  procured  from  the  Veterinary  Hospital  whose  gums  and 
outer  alveolar  process  were  almost  entirely  absorbed  with  pus 
exudate.  Street  dogs  selected  for  inoculation  were  forty-six  in 
number,  ranging  in  age  from  one  year  to  seven.  They  were  of 
all  breeds  and  conditions.  Some  were  well  fed,  others  very  thin. 
Many  had  sound,  healthy  gums  ;  others  had  slight  inflammation 

'  Micro-Orijanisms  of  the  Human  Mouth,  page  329 


126  INTERSTITIAL    GINGIVITIS. 

at  different  localities.  No  dog  was  used  whose  gums  and  alveolar 
process  had  become  infected  or  whose  tissues  were  absorbed.  Two 
dogs  were  operated  upon  at  a  time.  The  gum  was  separated  from 
the  necks  of  the  teeth  down  to  the  alveolar  jarocess  and  ^^eridental 
membrane  —  one  half  at  the  canine,  the  other  at  the  second 
pre-molar,  since  in  a  majority  of  cases  the  disease  began  at  the 
canine  tooth,  probably  on  account  of  its  prominence  and  the 
thinness  of  the  alveolar  process.  The  second  pre-molar  was 
selected  because  it  is  the  least  prominent.  The  secretions  about 
the  teeth  and  gums  of  the  diseased  dog  were  collected  upon 
a  platinum  wire  (previously  sterilized)  and  conveyed  to  the 
injured  parts.  Thirty-nine  healed  in  eight  days.  In  these 
the  gum  tissues  were  healthy.  The  pus  had  no  effect.  The 
wounds  healed  as  rapidly  as  any  wounds  possibly  could.  In 
seven  the  gums  were  inflamed  and  infection  occurred.  Su]3pura- 
tion  was  slight  in  four  and  considerable  in  three.  The  j^atho- 
logic  findings  in  these  cases  were  not  unlike  inflammation  and 
infection  in  other  tissues.  Similar  results  would,  no  doubt,  have 
taken  place  if  inoculation  had  been  performed  with  j)us  from  an 
abscess.  The  last  three  dogs  were  allowed  to  dej)art  at  the  end 
of  four  weeks  with  slight  pus  infection. 


CHAPTEE    XIII. 

.    SCORBUTIC    INTERSTITIAL    GINGIVITIS    IN   MAN. 

While  hundreds  of  slides  could  be  adduced  in  support  of  this 
chain  of  evidence,  sufficient  have  been  given  to  permit  of  the 
introduction  of  evidence  from  other  phases  of  the  subject. 

The  following  autopsy  was  made  by  L.  Hektoen  on  an  old 
man,  in  whose  case  the  pathologic  diagnosis  was  as  follows : 
Senile  marasmus  (senile  emphysema,  senile  sclerosis  of  the  aorta, 
atrophy  of  the  parenchymatous  organs),  scurvy  (hsemorrhagic 
gingivitis);  chronic  aortic  and  mitral  endocarditis;  fibrous 
myocarditis ;  chronic  nephritis ;  caseo-calcareous  areas  in  the 
right  apex,  spleen  and  left  adrenal ;  double  hydrothorax  ;  bron- 
chitis ;  fibroma  of  the  stomach ;  amputation  of  the  left  lower 
extremity  at  the  lower  third  of  the  thigh.  The  findings  unre- 
lated to  the  scope  of  the  present  investigation  are  omitted.  The 
gums  were  found  swollen,  and  here  and  there  infiltrated  with 
blood.  There  was  purulent  matter  about  the  roots  of  the  teeth, 
many  of  which  were  loosened  and  some  of  which  could  be 
removed  with  the  fingers.  The  roots  of  the  loosened  teeth  were 
covered  with  a  granular  grayish  material. 

Bacteriologic  examination  of  the  root  of  the  tooth  gave  the 
following  results :  Tube  of  bouillon  from  which  agar  j^lates 
Avere  made,  inoculated  twenty-four  hours  before  date,  July  29, 
1898.  There  were  two  varieties  of  colonies:  Both  grayish  white. 
One  kind  is  round,  pin-head  size,  slightly  elevated,  with  thin, 
wavy,  but  sharply  defined  border.  Finely  granular.  Media 
inoculated  from  one  of  these.  Ac/ar  Slant:  White,  tallow- 
like growth  along  the  track  of  the  needle,  with  thin,  more  trans- 
lucent layer  covering  the  rest  of  the  surface.  Only  moderately 
elevated.  Greenish  tinge  given  to  media.  Potato :  Elevated, 
"  clumpy "  growth,  white  on  top,  confined  to  needle  track. 
Potato  much  darkened.  Blood  Serum:  Gray,  waxy  growth, 
little  elevated,  sharply  defined  and  thick  border.  Gelatin  Slab  : 
Saucer-shaped  liquefaction  at  upper  part,  more  tulndar  in  deeper 


128  INTERSTITIAL    GINGIVITIS. 

jDortions.  Flocculent  masses  throughout.  Glucose  Agar:  Gas 
produced,  white,  thick  growth  on  top.  Milk :  Alkaline,  soft 
coagulation.  Botiillon  :  Cloudy.  Characteristics  :  Rapid  growth, 
a  sour,  nauseating  odor  given  oflF  from  all  media.  Morjihology  : 
Large  coccus,  single,  in  pairs  and  in  groups.  Stains  easily  by 
ordinary  methods,  also  by  Grams.  The  smaller  colonies  on  agar 
plates  (pin-point  sized  in  center)  with  nearly  transparent,  illy 
defined  peripheral  zone.  Border  indistinct.  Central  portion  in 
gray.  Finely  granular  throughout.  Agar  Slant:  Gray  film 
over  entire  surface,  somewhat  thicker  along  the  inoculation  streak. 
At  bottom  there  is  a  nearly  white  growth.  Very  light,  greenish 
tinge  to  media.  Blood  Serum  :  Like  on  agar.  Potato  :  Heavy 
dirty  gray  growth,  wavy  and  sharply  defined  border.  Looks  like 
bunch  of  cauliflower.  Gelatin  Slab  :  Liquefied,  saucer-shaped 
at  top,  tubular  in  deeper  part.  Growth  mostly  in  upjoer  stratum. 
Lit.  llilk :  Negative.  Bouillon :  Cloudy.  Glucose  Agar : 
Gas  i^roduced.  Characteristics :  Rapid  growth,  stinking  odor 
from  all  media.  Morpholoyy  :  Small,  slender  bacilli ;  actively 
mobile,  spores.  Takes  ordinary  stains  readily  and  is  not  decol- 
orized by  Gram's  method. 

Only  the  lower  frontal  teeth  and  corresponding  j^ai't  of  the 
jaw  could  be  examined.  The  epithelial  covering  of  the  gums 
appeared  to  be  quite  intact.  In  some  places  it  was  a  little  thick- 
ened, and  its  lower  layers  infiltrated  with  new  cells.  The  sub- 
epithelial tissue  was  much  thickened,  presenting  the  general 
structure  of  an  inflammatory  granulation  tissue  of  some  stand- 
ing. Areas  occurred  in  which  there  were  many  new  cells  and  but 
little  stroma.  In  other  foci  the  tissue  was  more  flbrous,  the  new 
cells  running  in  bands.  Here  and  there  occurred  free  and 
intracellular  granular,  yellow  pigment.  Typical  hyaline  bodies 
of  various  sizes,  and  staining  a  precise  bluish  violet  with  Gram's 
method,  were  found  in  rather  small  numbers.  In  some  jDlaces 
small  sub-epithelial  abscesses  were  met  with,  which  (in  the  instance 
of  a  district  including  a  lower  incisor)  were  really  subperiosteal. 
The  contents  consisted  of  nuclear  detritus  and  bacteria  (mostly 
cocci)  which  have  accumulated,  especially  upon  and  in  the  walls 
of  the  minute  cavities  extending  from  such  an  abscess.  There 
seems  to  be  a  complete  occlusion  of  the  vessels  (capillaries)  with 
typical  bacteria  masses,  staining  a  peculiar  bluish  violet  color 


X  40.    35  M.M.    Zeiss.    Micro-photograph,  reduced  one-third 

Fig.  50. — Longitudinal  Sechon  op  Tooth,  Alveolar  Process  and  Gingival  Border, 
Showing  Active  Inflammation  in  Scurvy  in  Man. 

B,    Dentine.        C,    Ceinentiim.        E,    Epithelial   Tissue.        G,    Submucous  Membrane. 

H,  Periosteum.    J,  Alveolar  Process.     L,  Haversian  Canals.    M,  Fibrous  Tissue.  V,  Violent 

Inflammation.       AA,    Point    of   Union    of   Epithelial    Tissue    and    Peridental  Membrane. 
RR,  Space  Pocket  from  Want  of  Union  of  the  Epithelial  Fold. 


X  40.    35  M.M.    Zeiss.    Micro-photograph,  reduced  one-third. 

Fig.  51.— Longitudinal  Section  of  a  Tooth,   Alveolar    Process  and    Gingival    Boeder, 
Showing  Active  Inflammation  in  Scurvy  in  Man. 

B,  Dentine.  C,  Cementum.  E,  Epithelial  Tissue.  G,  Submucous  Membrane.  V,  Violent 
Inflammation.  Z,  Sloughjng  of  the  Epithelial  Tissue  Due  to  Calcic  Deposits.  AA,  Point  of 
Union  of  Epithelial  Tissue  and  Peridental  Membrane. 


X  r.'i.     A.  A.  iil)j.     ZrisK.     MicrO'iihotograpti,  reduced  one-third. 

Fig.  52. — Longitudinal  Section  op  Tooth,  Alveolar  Process  and   Peridental  Membrane, 

Showing  Blood  Pigment  in  Blood  Ve.ssels  of  Peridental  Membrane  in  Scurvy  in  Man. 

i 

C,  Cementum.       J,  Alveolar  Process.       K,  Capillaries.       V,  Inflamed  Peridental  Membrane. 

K',  Blood  Pigment  in  Capillaries. 


X  75.    A.  A.  obj.    Zeiss.    Micro-pliotograpli.  reduced  one-third. 

Fig.  53. — Longitudinal  Section  of  Tooth  and  Gingival  Boeder,  Showing  Active  Inflam- 
mation Extending  thkough  the  Mucous  and  Peridental  Membranes.    Scurvy  in  Man. 

B,  Dentine.  C,  Cementum.  E,  Epithelial  Tissue.  V,  Violent  Inflammation.  AA,  Point 
of  Union  of  Epithelial  Tissue  and  Peridental  Membrane.  RR,  Space  Pocket  from  Want  of 
Union  of  Epithelial  Fold.    M',  Inflamed  Fibrous  Tissue. 


SCORBUTIC   INTERSTITIAL   GINGIVITIS    IN   MAN.  133 

with  hematoxylin,  and  blue  with  Gram's  method,  so  that  the 
vessels  i^resented  the  appearance  of  being  very  successfully  filled 
by  an  infection  mass  :  the  small  dilatations,  the  branches  and  the 
larger  vessels  (judging  from  structure  these  seemed  to  be  veins) 
were  sometimes  brought  out  very  nicely.  The  intravascular 
growth  of  bacteria  extended  into  the  bone  below  as  well  as,  and 
more  especially  into,  the  peridental  membrane.'  These  abscesses 
(suppurative  periostitis)  occur  almost  exclusively  upon  the  inner 
surface  of  the  alveolar  process,  being  confined  (as  far  as  there 
was  occasion  to  observe)  to  the  external  aspect  of  the  jsrocess. 
There  was  always  a  thin,  sound  layer  of  bone  separating  the 
abscess  from  the  peridental  membrane.  Very  generally  the 
spaces  in  the  adjacent  bone  were  filled  with  a  cellular  fibrous 
tissue  in  which  occurred  islands  of  osteoid  tissue.  The  bone 
trabeculse  were  generally  covered  by  a  thin  layer  of  osteoid 
tissue,  which  (from  the  greater  number  of  cells  it  contains,  as 
compared  with  the  other  bones)  must  be  newly  formed.  Rows  of 
osteoblasts  were  found  often  ujion  the  trabeculse.  Few  How- 
ship's  lacunae  were  found,  and  these  were  filled  with  small  cells. 
There  were  no  osteoclasts  in  the  areas  about  the  abscesses.  The 
bone  outside  of  the  alveolar  process  is  quite  unchanged. 

The  "bacterial  thrombosis  "  not  unusually  extended  into  the 
peridental  membrane,  which  then  refused  to  stain  as  clearly  as 
normal.  The  upper  Y)art  of  the  peridental  membrane  was 
usually  the  seat  of  cell  proliferation,  and  of  the  formation  of 
fibrous  tissue,  due  to  the  direct  extension  of  the  similar  process 
in  the  sub-epithelial  connective  tissue  of  the  gingivus.  There 
were  no  indications  that  the  process  began  below,  at  the  apex  of 
the  tooth,  for  example,  and  extended  upward.  In  the  peridental 
membrane,  and  often  connected  with  the  cementum  of  every  tooth 
examined,  were  very  many  so-called  calcospherites ;  calcified, 
concentrically  lamellated,  round  or  oval  bodies,  not  unlike  the 
"  corpora  amylacea."  In  many  instances,  it  seemed  as  if  the 
body  had  formed  in  the  cement  or  at  its  margin  —  the  cement 
presenting  here  a  nodular  condition. 

Fig.  50  illustrates  a  section  through  the  tissues  of  the  jaw 


'  The  abscesses  have  a  definite  outline  or  wall  of  ordinary  cellular  fibrous  tissue 
displaying  striking  evidences  of  active  inflammation.  The  tissue  about  the  capilla- 
ries filled  with  bacteria  refuse  to  stain  clearly,  but  there  are  no  signs  of  inflammation. 


134  INTERSTITIAL    GINGIVITIS. 

and  cusjjid  tooth.  The  epithelium  is  not  so  dense  and  thick  as 
in  a  similar  section  from  the  dog.  Inflammation  extends  along 
the  papillary  layer  of  the  submucous  membrane  (G)  and  involves 
the  deeper  structures.  The  mucous  membrane  layer  has  doubled 
ujion  itself,  formiilg  a  j)ocket  (R  R).  Violent  inflammation  is 
evident  at  V.  This  is  of  unusual  interest,  since  it  demonstrates 
that  inflammatory  products  may  be  carried  by  the  blood  vessels 
anywhere  throughout  the  alveolar  process,  and  may  result  in 
abscesses.  The  inflammation  extends  throughout  the  periosteum 
(H),  the  fibers  of  which  extend  from  the  root  of  the  tooth  over 
the  border  of  the  alveolar  process  (J).  There  the  coarse  fibers 
of  the  j)eriosteum  contrast  decidedly  with  the  finer  fibers  of  the 
sub-epithelium.  Absorption  and  contraction  of  the  alveolar  pro- 
cess (fully  one-half  the  length  of  the  root  of  the  tooth),  has  taken 
place,  as  well  as  lateral  absorjjtion.  The  inflammatory  process 
extends  through  the  Haversian  canals  (L). 

Fig.  51  is  a  section  through  the  jaw  at  the  lateral  incisor. 
The  epithelium  (E)  is  seen  upon  the  outer  surface  of  the  alveolar 
process  as  far  as  the  root  of  the  tooth.  The  inner  fold  next  to 
the  tooth  has  disappeared  through  encroachment  of  deposits 
which  have  been  destroyed  by  nitric  acid.  Inflammation 
extends  throughout  the  entire  submucous  membrane  (G).  The 
most  marked  inflammation  in  this  case  is  entirely  upon  the 
outer  border   (V). 

Fig.  52  shows  a  section  of  the  peridental  membrane  (I) 
and  alveolar  process  (J).  Capillaries  (K)  interlace  through 
the  field,  the  largest  number  being  distributed  along  the 
alveolar  wall.  Blood  ^ligment  containing  bacteria  are  notice- 
able (K'). 

Fig.  53  is  an  amplification  of  a  section  depicted  in  Fig.  50. 
This  gives  a  clearer  idea  of  the  folding  of  the  eiiithelium  (E) 
and  submucous  membrane  (G)  layer  upon  itself,  forming  a  pocket 
(RR),  in  which  may  be  seen  an  accumulation  of  food  and 
bacteria.  It  also  shows  extensive  inflammation  throughout  the 
entire  field.  Marked  inflammation  is  evident  at  V.  The  jjoint 
of  union  of  the  sub-epithelial  layer  and  the  periosteum  is  shown 
(AA). 

Fig.  54  illustrates  inflammation  of  the  peridental  membrane 
with  epithelial  debris  (W)  scattered  over  the  field.     Endarteritis 


X  V5.    A,  A.  obj.    Zeiss.    Micro-photograph,  reduced  one-third. 

Fig.   54. — Ckoss  Section  Peridental   Membrane,   Showing  Active  Round-Cell   Inflamma- 
tion.   Scurvy  in  Man. 

'C,  Cementum.    V,  Violent  Inflammation.    AV,  Epithelial  Debris.     EO,  Endarteritis  Obliterans. 
10  135 


X  75.    A.  A.  obj.    Zeiss.    Micro-photograph,  reduced  one-third. 

Fig.  55. — Cross  Section  op  Inflamed  Peridental  Membrane.    Scurvy  in  Man. 

I,  Peridental  Membrane.  J,  Alveolar  Process.  K,  Capillaries.  L,  Haversian  Canals 
BB,  Blood  Vessels  of  Von  Ebner  Preceding  Perforating  Canals.  EO,  Endarteritis  Obliterans 
W,  Epithelial  Debris. 


ISp 


X  ;5.    A.  A.  obj.    Zeiss.    Mioro-photograpli,  reduced  one-third. 

Fig.  56.—  Ckoss  Section  op  Tooth,  Alveolar  Phocess  and  Peridental  Membrane,  Showing 
Active  Infl.\mm.\tion  and  Absorption  op  Bone.    Scurvy  in  Man. 

C,  Cementum.    I,  Peridental  IMembrane.     J,  Alveolar  Process.    P,  Perforating  Canal  Absorp- 
tion.    V,  Violent  Inflammation. 


X  40,    35  M.M.  obj.    Zeiss.    Micro-iDhotograpli,  reduced  one-third. 

Fig.  57. — Cross  Section  op  Peridental  Membrane  and  Alveolar  Process,  Showing  Active 
Inflammation  and  Ab,sce.ss.    Sci'kvy  in  Man. 

J,    Alveolar  Process.       T,    Bacteria.       Y,    Abscess.        I',    Inflamed  Peridental  Membrane. 
L,  Inflammation  Extending  through  Enlarged  Havereian  Canals. 


X  75.    A.  A.  obj.    Zeiss.    Micro-photograph,  reciuced  one-third. 

Fig.  58.— Ceoss  Section  op  Peridental  Membrane  and  Alveolar  Process,  Showing  Active 
Inflajimation  and  Another  Larger  Abscess.    Scurvy  in  Man. 

J,  Alveolar  Process.  P,  Perforating  Canal  Absorption.  V,  Violent  Inflammation. 
Y,  Abscess.  I',  Inflamed  Peridental  Membrane.  L',  Inflammation  Extending  through  Enlarged 
Haversian  Canals. 


140 


INTERSTITIAL    GINGIVITIS. 


obliterans  (EO)   is  also   noticed  at  various  j)Ositions.     Marked 
inflammation  may  be  seen  at  V. 

Fig.  55  illustrates  a  section  of  the  peridental  membrane  (I) 
and  alveolar  process  (J)  with  inflammation  extending  through- 
out. Capillaries  (K)  are  also  noticeable  in  large  quantities, 
nearer  the  alveolar  process  than  the  root  of  the  tooth.  Epithe- 
lial debris  are  evident  at  W.     Endarteritis  obliterans  (EO)  may 


X  300.    Nu.  ;i  piujeciion  ocular.     D.  D.  obj.    Zeiss. 

Fig.  59. — Cross  Section  of  Tooth,  Alveolae  Proce,ss  and  Peridental  Membrane,  Showing 
Active  Inflammation  with  Calcospherite  in  Membrane.    Scurvy  in  Man. 

B,  Dentine.  C,  Cementum.  I,  Peridental  Membrane.  J,  Alveolar  Process.  HH,  Calco- 
spherite. J',  IntiamedtPerideutal  Membrane.  L',  Inflammation  Extending  through  Enlarged 
Haversian  Canals. 

be  seen  in  different  portions  of  the  field.  Inflammation  has 
extended  into  the  Haversian  canals  (L)  but  absorj)tion  has  not 
occurred  to  any  great  extent.  The  blood  vessels  of  Von  Ebner 
(BB)  are  quite  well  shown. 

Fig.  56  is  a  section  shoAving  the  cementum  (C),  the  peri- 
dental membrane  (I)  and  the  alveolar  process  (J).      Marked 


SCOKBUTIC    INTERSTITIAL    GINGIVITIS    IN    MAN.  141 

inflammation  extends  through  the  2)eridental  membrane,  thence 
through  the  Haversian  canals  (which  are  entirely  obliterated). 
Absorption  of  the  trabeculis  (halisteresis)  has  resulted  to  the 
extent  that  what  remains  of  the  alveolar  process  (J)  are  islands 
of  bone  held  in  place  by  the  fibrous  tissue.  Blood  vessels  of 
Von  Ebner  with  perforating  canals  are  seen  at  P. 

Fig.  57  shows  a  section  of  the  peridental  membrane  and 
alveolar  process  with  a  large  abscess  originally  within  the 
alveolar  wall.  Inflammation  spreading  through  the  peridental 
membrane  has  occurred  at  I',  while  the  decalcified  alveolar 
process  is  also  shown  (J).  Violent  inflammation  has  taken 
p)lace  within  the  alveolar  wall,  and  an  abscess  (Y)  has  formed. 
The  wall  of  the  abscess  is  distinctly  seen,  with  masses  of  bac- 
teria (T)  clinging  to  the  inner  sides.  The  process  of  halisteresis 
(Q)  (bone  decalcification)  is  seen  as  a  result  of  the  violent 
inflammation.  The  entire  wall  next  to  the  peridental  membrane 
and  about  the  abscess  has  been  destroyed,  and  the  diflferent  stages 
in  the  process  by  which  this  has  been  accomplished  are  beauti- 
fully shown. 

Fig.  58  illustrates  a  larger  abscess  (Y)  from  another  loca- 
tion. This  is  also  situated  within  the  alveolar  wall,  showing 
that  the  inflammatory  j^roducts  extend  through  the  blood  ves- 
sels. Marked  inflammation  is  seen  upon  the  side  next  to  the 
peridental  membrane  (I')>  while  rapid  absorption  —  halisteresis 
(Q)  and  perforating  canal  (P)  —  is  proceeding  at  the  borders 
of  the  abscess  and  nearest  the  alveolar  process. 

Fig.  59  shows  a  section  of  a  tooth  (B  and  C),  inflamed 
jjeridental  membrane  (I'))  with  absorption  of  the  alveolar  pro- 
cess (J).  In  the  inflamed  peridental  membrane  may  be  seen 
a  calcospherite,  oblong  in  form. 


CHAPTER   XIV. 

INTERSTITIAL    GINGIVITIS    IN    MAN    FROM    DRUG   ACTION. 

A  fortv-eight-year-old  merchaut  was  dysiDeptic,  debilitated 
and  asthmatic,  aud  for  the  treatment  of  these  conditions  he  had 
been  nndei-  calomel  and  tonics  for  a  little  less  than  two  weeks. 
When  he  came  nnder  observation,  the  mucous  membrane  and  gums 


were  then  much  inflamed.  There  was  marked  sialorrhoea.  The 
teeth  were  loose.  The  gums  were  swollen.  Pus  oozed  from  the 
gums.  The  breath  had  a  decided  metallic  odor.  At  mv  sugges- 
tion, his  medical  attendant  sto^^ped  the  calomel.  He  was  then 
ordered'  six  pints  of  spiring  water  daily.  The  gums  were,  on 
alternate  days,  saturated  with  iodin.  In  a  few  days  the  soreness 
and  swelling  were  so  reduced  that  the  deposits  could  be  removed. 
The  patient  was  discharged  cured  in  a  short  time  other  than  as  to 
the  right  inferior  second  molar,  which  was  so  loose  as  to  require 
removal.  This  tooth  was  j^laced  immediately  in  fifty  j^er  cent 
alcohol    for   twentv-four    hours  and   then    removed  to  absolute 


INTERSTITIAL    GINGIVITIS    IN    MAN    FROM    DRUG    ACTION.    143 

alcohol  for  twenty-four  hours  more.  The  membranes  had 
receded  about  two-thirds  the  length  of  the  root.  Sections  for 
microscopic  purposes  were  made  from  the  lower  third  of  the  root. 
Of  these  sections,  Fig.  60  shows  a  small  fragment  of  inflamed 
peridental  membrane.  Fig.  61  exhibits  violent  round-cell  inflam- 
mation, degeneration  and  liquefaction  of  tissue. 

A  thirty-flve-year-old  diabetic  painter  came  under  observation 
for  jihmibic  poisoning.  His  gums  were  swollen.  There  was 
decided  sialorrhoea.     The  teeth  were  loose.     Pus  flowed  from  the 


Fig.  G1. 


gums.  He  was  placed  on  ozonate  spring  water  and  the  gums 
were  saturated  with  iodin  on  alternate  days.  Three  loose  teeth 
were  removed  and  placed  in  alcohol.  Sections  from  the  upper 
third  of  the  left  superior  second  bicuspid  gave  results  on  micro- 
sco^jic  examination  similar  to  those  already  described  as  occurring 
in  mercurial  poisoning.  Fig.  62  shows  round  cells  of  inflamma- 
tion. Fig.  63  illustrates  very  marked  degeneration  of  the  peri- 
dental membrane.  In  the  lower  right-hand  corner  are  seen  the 
root  of  the  tooth,  dentine  and  cementum.     The  whole  surface  of 


144  INTERSTITIAL    GINGIVITIS. 

the  peridental  membrane  is  in  an  advanced  phase  of  inllamma- 
tion.  Just  at  the  border  of  the  root  is  evident  an  area  of  mem- 
brane softening.  Just  beyond,  but  joining,  is  noticeable  breaking 
■down  of  tissue.  In  the  center  are  seen  two  areas  of  softened 
tissue  more  advanced  in  degeneration. 

One  occupation  disease  >Yhich  has  been  ignored  in  the  etiology 
of  interstitial  gingivitis  is  "  brass-workers'  ague.".  In  almost  all 
brass-workers,  a  stain  varying  from  a  bright  to  a  brownish  green 
is  detectable  on  the  necks  of  the  teeth  between  the  croAvns  and 
the  gum  insertion.  This  is  most  obvious  in  the  upper  jaw. 
After    a   while,  as    E.   Hogben^  has   shown,  the  teeth    become 


Fig.  62. 

loosened  and  fall  out,  Before  these  changes  in  the  gum  occur 
nervous  symptoms  have  developed  from  the  brass  poisoning. 

Arsenic  should  be  taken  into  account  in  the  etiology  of  inter- 
stitial gingivitis.  This  drug  has  a  very  decided  tendency  in  cer- 
tain subjects  to  cause,  even  in  small  doses,  marked  stomatitis  and 
irritation  of  the  mucous  membranes  throughout  the  body. 

Tartar  emetic  and  the  other  preparations  of  antimony,  produc- 
ing irritation  of  the  mucous  membranes  of  the  mouth  and  else- 
where, may  act  as  predisposing  and  exciting  factors  of  interstitial 
gingivitis.^ 

'  Birmingham  Medical  Review,  1887. 
^  Lewin  :  Untoward  Effects  of  Drugs. 


INTERSTITIAL  GINGIVITIS  IN  MAN  FROM  DRUG  ACTION. 


145 


Among  the  drugs  which  shouhl  be  taken  into  account  in  the 
•etiology  of  interstitial  gingivitis  is  potassium  bromide.  Tliis 
produces  in  certain  indivichials,  or  when  given  to  excess,  marked 
increase  of  the  saliva  with  ii-ritation  of  the  mucous  membranes 
of  the  mouth,  followed  later  by  dryness  of  the  mouth  and  shrink- 
ing of  the  gums.  The  bromides  have,  as  H.  C.  B.  Alexander' 
has  shown,  a  tendency  to  irritate  all  the  mucous  membranes  of 
the  body  as  well  as  the  skin.  Therefore,  in  dealing  with  cases 
•of  interstitial  gingivitis  in  which  the  bromides  are  being  taken, 
this  factor  should  not  be  neglected.     In  these  cases  the  symptoms 


■tine  to  the  bromides  are  apt  to  be  charged  to  the  nervous  state  for 
which  the  bromides  have  been  given.  The  irritation  of  the 
nuicous  membrane  by  the  liromides  may  occur  quite  early  among 
the  untoward  effects  produced  by  them.  In  all  probability  the 
bromine  rather  than  the  alkali  is  the  source  of  these  untoward 
■effects. 

What  is  true  of  the  bromides  is  also  true  to  an  even  greater 
degree,  as  has  elsewhere  been  shown,  of  the  iodides. 

'  Alienist  and  Neurologist,  July,  1S9(!. 


CHAPTER  XV. 

CONCLUSIONS. 

"While,  as  ali'eady  shown,  the  teeth  originated  in  the  epider- 
mis, still,  even  as  early  as  the  sharks,  the  teeth  of  the  mouth 
departed  from  this  primitive  method  of  development,  since  they 
did  not  arise  on  the  surface,  but  deep  down,  as  Minot'  has 
pointed  out.  As  Hertwig  has  shown,  this  occurs  because  the 
dentiferous  epithelium  grows  down  into  the  dermis,  forming  an 
oblicjue  shelf,  which  may  be  regarded  as  a  sj)ecial  tooth-forming 
organ.  On  the  under  side  of  the  shelf  the  teeth  are  developed 
in  the  same  way  as  over  the  skin,  although  they  are  much  larger. 
The  teeth  are,  however,  in  various  stages  of  develojjment,  and 
only  one  is  fully  exposed ;  when,  as  happens  in  time,  it  is  lost, 
the  next  tooth  behind  rej^laces  it.  Since  the  production  of  new 
tooth  germs  goes  on  in  adult  life,  replacement  of  the  tooth  in  the 
shark's  jaw  continues  indefinitely ;  hence  sharks  are  termed 
polyjihyodont.  Mammals,  having  two  sets  of  teeth  only,  are 
called  diphyodout.  There  is,  therefore,  even  in  mammals  where 
the  change  is  limited,  a  tendency  to  change.  Since  the  human 
being  and  the  higher  mammals  (noticeably  the  omnivora,  like 
dogs,  whose  food  is  as  varied  as  that  of  man)  are  born  jjractically 
toothless,  this  struggle  begins  between  the  teeth  at  a  later  time 
than  in  the  lower  vertebrates. 

The  teeth  are  temporary  structures,  intended  to  be  shed  at 
certain  times ;  the  temporary  set  ere  the  onset  of  puberty,  the 
permanent  with  the  onset  of  senile  involution  at  the  jDremonitory 
jieriod  of  old  age.  This  last  period  depends  on  the  individual 
rather  than  the  number  of  years  lived.  At  the  senile  j^eriod, 
which  may  occur  at  any  time  after  the  eruption  of  the  perma- 
nent set,  osteomalacia  (which  is  the  normal  absorption  of  the 
alveolar  process)  may  take  place.  The  period  at  which  this 
commences  de^^ends  upon  the  constitution  of  the  patient. 
Through  congenital  defect  or  disease,  senility  may  begin  earlier 

'  Human  Embryology. 


coNCLusioisrs.  147 

in  life.  In  certain  types  of  degeneracy  (precocity,  for  example), 
senility  with  absorption  of  the  alveolar  process  may  begin  even 
at  twenty.  Absorption  of  the  alveolar  process  and  loss  of  the 
permanent  teeth,  is,  therefore,  certain  at  a  period  dependent 
upon  the  constitution  of  the  patient.  Between  these  two  periods, 
birth  and  senility,  two  sets  of  teeth  have  been  furnished  man. 
In  the  meantime,  the  alveolar  process,  the  gums,  periosteum, 
peridental  membrane,  blood  vessels,  nerves,  have  come  and  gone 
to  suit  the  convenience  of  these  two  sets  of  teeth.  Tissues  like 
these  are  called  adventitious  or  transitory.  Adventitious  tissues 
are  much  more  apt  to  be  affected  by  disease  than  permanent  in 
type  and  persistent  in  function. 

As  transitory  structures,  destined  to  fulfill  temporary  jjur- 
poses,  the  teeth  of  necessity  tend  to  decrease  in  number  with 
advance  in  development  for  the  benefit  of  the  organism  as  a 
whole,  thereby  preventing  waste  of  nutriment  on  useless  struc- 
tures. The  shapes  of  teeth  hence  vary  in  order  to  adapt  them- 
selves to  the  work  and  surroundings  produced  by  evolution. 
The  teeth  and  its  setting  being  of  different  structures  and  com- 
position, each  proceeds  to  destruction  along  lines  imposed  by  the 
laws  of  its  structure.  The  tooth  is  destroyed  by  decay,  the 
alveolar  process  by  inflammation.  Decay  of  the  tooth  and  inter- 
stitial gingivitis  are  expressions  of  that  natural  line  of  involution 
which  is  foreshadowed  from  the  outset  in  both  by  laws  of  their 
development.  The  laws  governing  transitory  structures  natu- 
rally place  these  at  the  mercy  of  both  under  and  over  stimulation. 
From  its  jjosition,  location  and  functions  the  mouth  is  of  neces- 
sity exposed  to  invasion  of  microbes.  These  tend  directly  and 
indirectly,  from  infection  and  through  their  toxins,  to  aggravate 
the  effects  of  both  under  and  over  stimulation.  Not  only  do  the 
very  structure  and  embryogeny  of  the  teeth  and  alveolar  process 
expose  them  to  the  too  early  onset  of  the  processes  of  removal, 
initiated  by  under  and  over  stimulation,  but  these  last  increase 
and  are  increased  by  the  local  results  of  constitutional  defects, 
like  idiocy,  and  diseases,  like  tabes  dorsalis,  paretic  dementia, 
and  allied  disorders,  as  well  as  the  results  of  injuries  to  the  jaw. 

When  more  work  is  required  of  one  tooth  (as  when  the 
dental  arch  is  broken  by  the  loss  of  one  or  more  teeth,  and  the 
others  have  moved  out  of  their  normal  jiosition,  or  when  a  seam- 


148  lyXEESTITIAL    GINGIVITIS. 

stress  bites  her  thread  with  one  or  more  teeth,  or  when  plates  are- 
attached  or  come  in  contact  with  natural  teeth,  or  when  a  piece 
of  bridgework  is  adjusted)  and  the  roots  of  one  or  two  teeth 
must  supjjort  and  do  the  work  of  a  greater  number,  this  charac- 
ter of  adventitious  structure  j^redisjDOses  to  inflammation  about 
the  root  or  roots  of  the  teeth. 

When  due  to  irregularities  of  the  teeth,  or  when  antagonizing 
teeth  have  been  extracted,  or  in  the  mouths  of  idiots,  paretic 
dements,  etc.,  who  do  not  use  their  teeth,  understimulation  also 
predisposes  to  inflammation. 

The  mass  of  evidence  previously  jjresented  demonstrates  that 
the  causes  of  interstitial  gingivitis  are  divisible  into  predisposing 
causes  (which  may  be  subdivided  into  local  predisposing  and  con- 
stitutional) and  exciting  causes.  The  exciting  causes  are  either 
constitutional  or  local,  but  as  a  rule  are  local  or  have  local  action. 

The  predisposing  factors  of  this  disease,  as  already  men- 
tioned, are  :  conditions  of  jaw  evolution,  transitory  nature  of  cer- 
tain structures,  degeneracy  and  conditions  of  previous  irritation 
and  inflammation. 

Moreover,  in  accordance  with  a  general  law  of  j^athology 
whereby  tissues  (for  example  the  lungs  in  pneumonia  once 
attacked  by  toxic  agencies  or  even  by  the  toxins  of  germs) 
acquire  a  local  predisposition  to  future  attacks  of  disease,  the 
gums  and  alveolar  process  often  become  thus  susceptible  to  con- 
stitutional and  local  influences. 

It  is  obvious  from  the  data  given  in  the  chaj^ter  upon  "  His- 
tory "  that  interstitial  gingivitis  is  as  old  as  man  and  that  it  was 
observed  and  discussed  by  the  earliest  writers  on  medicine^ 
While  it  is  l)y  no  means  improbable  that  constitutional  factors 
assisted  in  its  early  progress  in  man,  still  the  exciting  cause  of 
this  disease  was  tartar.  Many  skulls  from  prehistoric  jjeriods. 
exhibit  gingivitis  wpon  the  teeth  exposed  to  the  influence  of  tar- 
tar. This  gingivitis  extends  along  the  roots  nearly  or  quite  to 
the  apices,  resulting  in  absorjDtion  of  the  alveolar  process.  Upon 
the  surface  of  the  teeth  where  tartar  is  absent,  interstitial  gingi- 
vitis and  absorption  rarely  occur.  The  same  is  true  of  the 
teeth  of  wild  animals  at  large  and  confined  in  zoological  gardens. 
In  them  gingivitis  from  local  conditions,  other  than  tartar,  very 
seldom  occurs.     The  jaws  of  the  skulls  of  prehistoric  periods  are 


CONCLUSIONS.  149 

always  broad,  measuring  2.25  to  2.50  inches  in  diameter.  Third 
molars  are  always  present.  The'  vaults  are  very  low,  the  alveolar 
j)rocess  short  and  thick,  and  the  teeth  short.  As  already  shown 
in  the  chapiter  on  the  "Alveolar  Process,"  the  jaws  have  been 
growing  smaller  until  they  range  in  diifereut  races  from  2.50  to 
1.75  inches  in  diameter.  Mixed  Celto-Teutouic^  races,  like  the 
English-speaking  peoples  and  the  Scandinavian  i^eoples,  have  the 
smallest  jaws  with  the  most  marked  deformities  as  a  result. 
These  changes  in  jaw  forms  occur,  as  has  been  elsewhere  shown, 
in  harmony^  with  the -law  of  evolution  of  the  race  in  face  forms. 
With  these  changes  in  jaw  diameter  there  also  occurs  an  altera- 
tion in  the  antero-posterior  diameter.  A  change  in  tooth  forms 
also  occurs.  Small  crowns  and  long  roots  replace  large  broad 
crowns  and  short  roots. 

These  changes  necessarily  alter  the  shape  and  form  of  the 
alveolar  processes.  Instead  of  being  short  and  broad,  they 
become  long  and  thin.  The  septum  between  roots  is  not  as  wide, 
thick  or  heavy  as  formerly.  The  long,  thin  alveolar  process  is- 
more  subject  to  the  influence  of  local  irritation  and  trophic 
change  than  the  short,  thick  one.  A  long,  thin  alveolar  process 
will  be  more  readily  absorbed  than  a  short,  thick  one.  This  is 
demonstrable  Avhere  the  roots  of  the  teeth  are  situated  near  the 
outer  border  of  the  process.  Disease  of  the  peridental  membrane 
and  absorjDtion  of  the  outer  plate  extends  along  the  roots,  expos- 
ing them  throughout  their  entire  length.  Similar  conditions  are 
noticeable  along  the  palatine  roots  of  the  molar  teeth  in  the 
upper  jaw. 

From  the  length  and  thinness  of  the  alveolar  process  result- 
ant on  the  evolution  of  the  jaws,  the  periosteum  on  one  side 
and  the  peridental  membrane  on  the  other  hold  the  structures 
together  and  afford  nourishment  for  the  tooth  and  bone  tissues. 
The  blood  vessels  pass,  as  elsewhere  shown,  in  a  vast  plexus  from 
the  periosteum  to  the  peridental  membrane  through  the  ^^I'ocess. 
This  plexus  deposits  and  removes  calcium  salts.  Potent  for  good 
under  normal  conditions,  it  is  equally  potent  for  evil  under  states- 
of  irritation  and  disturbed  nutrition.     Local  irritation  is  greatly 


'  Keane,  Ethnology. 

-Degeneracy  :  Its  Causes,  Signs  and  Results  (Talbot). 

Osseous  Deformities  of  the  Head,  Face,  Jaws  and  Teeth  (Talbot). 


150  CONCLUSIONS. 

assisted  by  a  peculiar  structural  variation  of  the  gum  tissue  (R 
R,  see  any  figure);  accumulation  of  debris  and  resultant  chemi- 
cal decomposition  producing  inflammation. 

Tartar  is  an  active  source  of  local  irritation  and  inflammation 
of  the  gum  margin.  This  in  turn  extends  through  the  capilla- 
ries to  the  alveolar  process.  Calcic  deposits  are  a  result  and  not 
a  cause. 

A  predisposing  cause  for  local  inflammation  is  that  of  approx- 
imal  tooth  decay  or  cutting  away  the  apj)roximal  surfaces  for  the 
purpose  of  filling  this  class  of  cavities.  If  the  teeth  be  not  so 
contoured  (Bonwill)  as  to  retain  them  in  their  proper  positions, 
absorption  of  the  alveolar  process  between  the  roots  will  take 
]3lace,  thus  bringing  the  crowns  in  contact.  The  result  of  such 
absorption  will  restrict  bone  surface  for  the  protection  and  nour- 
ishment of  the  gum  tissue.  Undernourished  tissues  are  hence 
more  liable  to  irritation  and  inflammation. 

When  death  of  the  pulp  occurs,  the  teeth  often  become  loose 
without  inconvenience  to  the  patient.  This  results  from  the  for- 
mation of  gases  in  the  pulp  chamber,  which  sufiice  to  produce 
inflammation  of  the  peridental  membrane  with  or  without  pain. 
This  occurs,  since  slight  irritation  only  is  needed  to  produce 
absorption  of  the  alveolar  process,  at  the  apicial  end  of  the  root. 
Chronic  inflammation  of  the  peridental  membrane  and  the 
flbrous  tissue  of  the  alveolar  process  occurs.  The  teeth  finally 
become  loose.  Irritation  from  movements  of  the  tooth  increase 
the  inflammation  through  the  Haversian  canals  and  further 
absorption  takes  place,  until  the  tooth  is  exfoliated. 

This  disease  from  the  onset  of  gum  inflammation  may  proceed 
for  years  without  pain.  Indeed,  not  until  the  formation  of 
abscess,  or  until  absorption  has  affected  the  nerve  at  the  end  of 
the  root  does  pain  occur.  Slight  soreness  may  be  felt  after  the 
tooth  begiias  to  loosen.  Absorption  of  the  alveolar  process  and 
exfoliation  of  the  tooth  may  occur  without  any  pain  whatever. 

In  the  chapter  upon  "  Transitory  Structures,"  it  has  been 
shown  that  the  alveolar  processes  have  their  structures  arranged 
to  accommodate  the  teeth.  When  the  teeth  are  extracted,  the 
alveolar  j^rocess  becomes  entirely  absorbed.  The  periosteum, 
peridental  membrane  and  fibrous  tissues  are  entirely  lost.  The 
mucous  membrane  and  gum  tissue  so  contract  that  none  of  the 


CONCLUSIONS.  151 

original  struc'turc  remains.  Absorption  of  the  alveolai'  process  is 
very  eomnion  in  advanced  age.  Even  when  the  teeth  remain  in 
the  jaw  in  old  age,  whether  of  man  or  animal  (this  is  es^^ecially 
noticeable  in  old  dogs),  absorption  of  the  alveolar  process  con- 
tinues. This  is  due  to  the  fact  that  the  alveolar  jirocess,  esi^ecially 
when  long  and  thin,  is  composed  of  cancellated  bone  structure 
which  is  easily  acted  upon  by  its  abundant  blood  and  lymph  sup- 
ply. This  produces  absorption  upon  the  slightest  stimulation  or 
irritation  of  nerve  fibers.  Even  such  slight  factors  as  heat,  brain 
overstrain,  and  want  of  proper  articulation  and  occlusion  and 
imjjlantation  of  the  teeth,  suffices  so  to  stimulate  the  nerve  fibers 
as  to  jDroduce  absorj^tion.  There  are  four  varieties  of  absorption  ; 
osteoclast  or  lacunar  absorption,  penetrating  canal  absorption, 
halisteresis,  and  osteomalaciary  absorption.  These  have  already 
been  beautifully  shown  in  the  illustrations.  It  is,  therefore,  not 
astonishing  that  the  slightest  local  irritation  or  tissue  nutrition 
disturbance  from  constitutional  causes  suffices  to  jDroduce  local 
tissue  change.  This  unstable  condition  of  structures  tends  to 
j)revent  successful  implantation  of  teeth. 

The  question  has  arisen  whether  there  exists  a  specific 
bacterium,  which  bears  the  same  relation  to  the  pyorrho?ic 
stage  that  the  strej^tococcus  does  to  streptococcus  diphtheria. 
This  question,  raised  by  Galippe,  must,  in  the  light  of  careful 
research,  be  regarded  as  settled  in  the  negative.  No  special 
bacterium  has  been  found  which  complies  Avith  the  laws  of  Koch. 
Dogs  are  liable  to  this  disease.  Galippe  had  but  to  infect  their 
gums  with  his  bacterium  to  demonstrate  its  s^jecific  pathogenic 
activity.  He  has  not  done  this.  As  the  researches  (already 
cited)  also  failed  to  find  a  bacterium  which  could  comply  with 
this  test  required  by  the  laws  of  Koch,  it  must  be  admitted  that 
there  is  no  bacteriologic  evidence  of  a  sj^ecific  bacterium. 
Furthermore,  the  pathologic  evidence  demonstrates  that  bacteria 
23lay  the  very  subordinate  role  in  this  disease  that  they  do  in 
ordinary  wound  infection. 

PATHOGENESIS    OF    INTEKSTITIAE   GINGIVITIS. 

Inrianiniation  of  the  gums  and  deeper  structures  chiefiy 
results  from  mechanic  and  chemic  (lactic  and  uric  acid,  ])Otas- 
sium  iodide,  mercury,  etc. )  causes,  bacterial  influence  being  an 

11 


152  I]S'TEESTITIAL    GINGIVITIS. 

incidental  complication.  From  their  action,  the  blood  stream  is 
increased  and  dilatation  of  the  capillaries  is  produced.  The 
capillaries  become  crowded  with  blood  corpuscles.  These 
accumulate  along  the  walls  of  the  blood  vessels,  to  which  they 
appai'ently  adhere.  Accumulations  of  small,  round  cells  occur, 
in  the  submucous  connective  tissue,  the  spaces  of  which  are 
filled  with  inflammatory  exudate.  The  papillte  become  enlarged. 
The  epithelial  layer  becomes  hyperplastic.  As  a  result,  the  gum 
tissues  swell  and  become  intensely  crimson.  They  bleed  upon 
the  slightest  touch. 

Inflammation  may  be  confined  to  a  single  point  upon  the 
side  of  a  tooth.  This  localization  often  results  from  predisposi- 
tion due  to  a  local  injury,  originating  in  a  cavity  in  the  tooth 
■with  sharp,  rough  edges,  from  overlapping  fillings  or  from  too 
frequent  and  violent  use  of  the  toothpick  at  one  point.  As  a 
result,  granulation  tissue  forms,  which  (according  to  Sudduth)  is 
often  due  to  the  irritation  of  lactic  acid.'  In  the  production  of 
this,  however,  the  influence  of  the  lactogenic  bacteria  on  particles 
of  food  cannot  be  excluded. 

The  peculiar  formation  of  the  gum  tissue  on  the  inner  border 
of  the  gingivus  into  a  pocket  or  cul-de-sac  (RR  in  Figures)  here 
described  for  the  first  time,  is  a-  fertile  source  of  this  irritation 
and  consequent  inflammation,  from  its  collection  of  resultant 
decomposition  of  foods.  This  pocket  varies,  as  has  been  shown, 
in  size  as  well  as  locality.  Sometimes  it  is  very  large  and  deep, 
or  it  may  be  almost,  if  not  entirely,  obliterated.  Frequently  it  is 
situated  near  the  gum  margin,  again  near  the  union  of  the  sub- 
nnicous  and  peridental  membranes.  The  degenerate  epithelium 
cell  structure  (so-called  glands  of  Serres)  is  also  more  liable 
and  more  easily  irritated  than  the  normal  epithelium  structure. 
As  in  the  similar  crypts  of  the  penis,"  the  degeneration  and 
death  of  the  epithelial  cells  with  which  this  cavity  is  lined 
produce  liy  their  accumulation  a  source  of  irritation  as  well 
as  culture  medium  for  jjathogenic  bacteria.  Therefore,  not 
only  is  the  anatomical  arrangement  of  the  structures  a  fruit- 
ful  source   for  the    accumulation    of   irritative   substances,   but 

'  I  have  made  examinations  of  pockets  about  the  necks  of  teeth  and  can  cor- 
roborate  this  statement. 
2  Medicine,  1898. 


coxcij'sioxs.  15B 

the  structures  tlicmsclvcs   ai'c  also   well    adapteil    tnr    intlainina- 
tory  action. 

The  gum  tissue  abuut  one  or  more  teeth  may  be  iujurecl  by  a 
badly  fitted  gohl  crown,  with  rough  edges.  The  gokl  crown  may 
be  too  far  down  on  the  I'oot.  Injury  may  result  from  ligatures, 
rubber  dam  and  bands  left  about  the  teeth  after  operations. 
Accumulations  of  tartar  or  any  local  irritation  may  lead  to 
inflammation  varying  with  the  extent  of  the  dej^osit.  The  extent 
of  the  inflannnation  will  depend  upon  the  nature  and  duration  of 
the  irritating  influence.  If  it  l)e  local  in  action  and  temporary, 
slight  gingivitis  results.  If  it  be  permanent,  gingivitis  assumes 
a  chronic  type,  extends  into  the  fibrous  tissue  below  and  becomes 
interstitial  in  character.  The  extent  of  this  interstitial  inflam- 
mation depends  upon  the  nature  of  the  irritation.  If  the  irrita- 
tion be  located  upon  the  side  of  one  tooth,  the  inflammation  will 
extend  through  the  filjrous  tissue  in  the  direction  of  the  course  of 
the  blood  vessels.  It  may  be  in  line  with  the  peridental  mem- 
brane. It  may  be  in  line  with  the  periosteum,  or  it  may  be 
in  direct  line  with  the  alveolar  process.  Interstitial  inflammation 
(if  one  or  more  teeth  be  iuvolved)  extends  not  only  through  the 
peridental  membrane,  but  to  the  periosteum  and  alveolar  process 
as  well,  since  the  capillaries  in  surrounding  structures  are  in- 
volved. The  inflammation  extends  into  the  alveolar  jjrocess 
through  the  Haversian  canals  and  the  blood  vessels  of  Von  Ebner 
by  way  of  the  periosteum  and  peridental  membrane.  Irritation 
thereon  resultant  causes  absorption  of  the  alveolar  process  by  (  a  ) 
halisteresis,  (b)  Volkmann's  perforating  canals,  (c)  lacunar 
absorption  (osteoclasts).  The  interstitial  inflammation  and  the 
absorption  of  the  alveolar  process  continues  so  long  as  the  irrita- 
tion remains  or  until  the  tooth  or  teeth  are  exfoliated.  Previous 
irritations  often  produce  osteom.dacia  and  trophic  changes,  and 
thus  assist  greatly  the  progress  of  the  pathologic  phenomena. 
Loosening  of  the  tooth  or  teeth  adds  a  very  efiicient  irritation 
which  increases  the  extent  of  and  intensifies  the  inflammation. 
Loosening  of  the  teeth  is  their  death  knell,  no  matter  what  the 
original  cause  for  the  disease  may  have  been. 

The  following  complications  may  occur  :  Endarteritis  Oblit- 
erans, Absorption  of  the  Alveolar  Process,  Pyorrhoea  Alveolaris, 
and  finally  Calcic  Deposits. 


154  INTERSTITIAL    GINGIVITIS. 

ENDAETEEITIS    OBLITEKANS. 

Endarteritis  is  an  inflammation  of  the  internal  coat  of  an 
artery  or  ca|3illary,  generally  of  elironic  type.  Its  pathogeny  is 
as  follows :  In  direct  contact  with  the  blood  streams  is  the 
endothelinni  (a  layer  of  flattened  cells);  next  is  the  tunica 
intima,  comjjosed  of  elastic  fibers  arranged  longitudinally  ;  next 
comes  the  middle  coat,  composed  of  muscular  fibers  arranged 
transversely.  The  outer  coat  consists  of  longitudinal  connective 
tissue,  Avhich  contains  the  vasa  vasorum.  In  the  capillaries,  the 
intima  lies  in  immediate  contact  with  the  surrounding  tissues,  or 
accomj^anied  by  a  rudimentary  adventitia.  In  other  words,  the 
walls  of  the  capillaries  consist  of  almost  nothing  but  the  intima. 
The  cajoillaries  have  certain  contractility;  they  contract  or 
dilate  without  muscular  fibers.  The  veins  probably  also  have  a 
certain  amount  of  contraction  and  dilatation  from  irritability  of 


,  / 


?-\N    ..J 


Fig.  64. —  Endarteritis  Obliterans  (Kaufmann). 

A,  Adventilia.       E,  Elastic  Tissue  between  Middle  Coat  and  Intima.       M,  Muscular. 
J,  Thickened  Intima. 

the  intima.  Each  coat  of  the  arteries  takes  on  s^Decial  tyjie  of 
inflammation.  The  causes  of  endarteritis  are  numerous.  Inflam- 
mation of  the  intima  of  the  blood  vessels  may  be  due  to  irritation 
from  without  or  within. 

When  it  occurs  from  without,  any  local  irritation  will  set  up  . 
an  inflammation  which  may  extend  to  the  outer  coats  of  the  cap- 
illaries. This  i^roduces  a  marked  increase  of  blood.  The  vasa 
vasorum  becomes  swollen,  the  white  blood  corpuscles  crowd  into 
the  terminal  capillaries  and  migrate  into  the  extra  vascular 
sj^ace.  Rapid  proliferation  of  the  round-cell  elements  takes 
place.  The  walls  of  the  vessels  become  thickened.  Owing  to 
the  projecting  intervals  of  the  intima,  the  caliber  of  the  blood 
vessels  diminishes  (Fig.  64). 


CONCLUSIONS.  155 

Irritation  occurring  from  witliin,  results  either  from  trophic 
changes  in  the  system  from  direct  irritation  from  toxjemias,  or 
from  both  interdependently.  Under  these  circumstances  a  germ 
disease  or  other  toxins  may  liave  an  affinity  for  a  certain  organ, 
tissue  or  part,  and  produce  irritation  in  the  capilhiries  in  a  dis- 
tinct part  of  the  body,  or  the  capillaries  through  the  entire  body 
may  become  involved.  Thus,  in  typhoid  fever,  the  Peyer's 
gland  in  the  intestine  becomes  involved ;  in  scarlet  fever,  the 
skin  or  kidney ;  in  malaria,  the  liver  and  spleen ;  in  Bright's 
disease,  the  kidney ;  while  in  mercurial  and  lead  poisoning  and 
scurvy,  the  mucous  membrane,  and  esiDecially  the  gums,  become 
diseased.  In  many  of  these  conditions,  however,  before  the 
tissue  already  irritated  becomes  involved,  the  nervous  system  has 
become  affected.  The  nervous  system  may  already  have  become 
affected  from  other  causes.  Thus,  locomotor  ataxia,  traumatic 
injuries  to  the  spine,  paretic  dementia,  cerebral  paralysis,  neu- 
roticism  and  degeneracy,  and  last,  but  not  least,  stomach  neuras- 
thenia. The  poison  in  the  bloody  together  with  the  diseased 
Ijeripheral  nerves,  produce  irritation  and  inflammation  of  the 
inner  coat  of  the  capillaries.  If  this  irritation  does  not  disap- 
pear soon  after  its  inception,  the  inflammation  tends  to  affect  the 
other  coats  of  the  blood  vessels.  Under  certain  conditions, 
endarteritis  may,  however,  never  involve  the  other  coats  of  the 
vessels.  When  irritation  of  the  inner  coat  of  the  capillaries 
takes  place,  p)i'oliferation  of  the  endothelium  occurs.  This 
inflammatory  growth  tends  to  obstruct  the  lumen  of  the  vessel. 
The  media  may  likewise  become  thickened  by  an  increased  con- 
nective tissue.  The  capillaries  become  obstructed,  and  finally 
obliterated.  This  finally  impedes  the  circulation.  Fig.  65 
shows  such  a  condition  in  the  scurvy  case,  elsewhere  illustrated. 

Irritation  may  be  of  less  intensity  but  greater  duration,  as  in 
case  of  syphilis,  tuberculosis,  scurvy,  mercurialism,  plumbism 
(lead  poisoning),  etc.,  and  the  results  are  then  slowly  effected. 
Proliferation  of  sub -endothelial  connective  tissue  gradually 
increases  until  it  reaches  its  limit  (endarteritis  obliterans).  This 
influence  of  the  proliferation  is  exerted  in  addition  to  that  of  the 
round-cell  infiltration  about  the  structure. 

The  recent  studies  of  Hektoen'  on    menino-eal  tuberculosis 


'American  S3'stem  of  the  Practice  of  Medicine,  page  119. 


156  INTEESTITIAL    GINGIVITIS. 

demonstrate  that  tubercle  bacilli  may  penetrate  the  unbroken 
endothelial  layers  of  the  vessel  and  stimulate  marked  pi-oliferation 
of  the  sub-endothelial  connective  tissue.  An  internal  irritant, 
such  as  may  be  2jroduced  in  the  course  of  any  infectious  disease 
or  from  suboxidation,  probably  acts  uj)on  the  endothelium  of  the 
walls  of  the  smaller  blood  vessels  in  such  a  way  as  to  permit  the 
escape  through  the  walls  first  of  serum,  then  of  leucocytes,  the 


X  Ino.     D.  D.  obj.    Zeiss. 

Fig.  6o. — Cross  Section  of  Peridental  Membrane,  Showing  Endarteritis 
Obliterans.     Scurvy  in  Man. 

C,   Cementum.         D,   Dentine.         I,   Peridental   Membrane.         V,   Nerve  Tissue. 
EO,  Endarteritis  Obliterans. 

latter  infecting  and  surrounding  the  vessels.  The  effect  of  the 
chronic  endarteritis  is  to  check  the  blood  supply  to  the  gum 
tissue.  Mercury,  lead  and  other  poisons  circulating  througli  the 
blood  are  forced  to  remain,  hence  discoloration  of  tissue  along  the 
gum  margin.     Interstitial  gingivitis,  resulting  in  a  slow  disturb- 


CONCLUSIONS.  157 

ance  of  uutritioii,  piddiices  overgrowth  of  connective  tissnc.  In 
all  cases  of  clironir  interstitial  gingivitis,  as  shown  in  the  illus- 
tration, cwv  the  hlood  vessels  thus  involved. 

Among  the  pretlispt)sing  influences  which  cause  this  disease 
are  syphilis,  tuberculosis,  mercurialism,  plumbism,  brass  poison- 
ing, lithagmia,  nephritis,  gout,  rheumatism,  alcoholism,  scurvy, 
nervous  diseases,  jjregnancy  and  old  age.  Under  certain  con- 
ditions of  the  system  any  and  all  diseases  which  tend  to  lower  the 
vitality,  producing  antemia,  will  assist  in  producing  this  disease. 
The  direct  cause  may  be  resultant  overstrain  of  the  blood  vessels. 

Owing  to  obliteration  of  the  arteriols  in  the  alveolar  process 
stasis  of  blood  nuist  follow.  The  detritus  from  the  alveolar  pro- 
cess, therefore,  must  remain  in  tlie  tissue  and  collec-t  upmi  the 
roots  of  the  teeth. 

ABSOKPTIOX    OF    THE    ALVEOLAR    PROCESS. 

Absorption  of  the  alveolar  process  is  the  result  of  irritation, 
resultant  malnutrition,  and  subsequent  inflammation.  The  osteo- 
blasts and  osteoclasts  are  ever  present  to  build  up  and  tear  down 
bone  structure  on  the  slightest  provocation.  Hypertrophy 
(building  up  of  bone  tissue )  is  the  result  of  intermittent  pressure, 
and  atrophy,  or  absorption  of  bone,  is  due  to  constant  irritation 
and  pressure.  As  has  been  elsewhere  shown,  from  its  transitory 
nature  the  alveolar  process  is  unusually  susceptible  to  these  influ- 
ences. The  causes  of  absorption  are  loss  of  teeth  liy  exti'action, 
undue  pressure  upon  one  or  more  teeth  from  improper  articulation 
(  Bonwill ),  wedging  and  ii'regnlarity  correction,  heat  under  arti- 
ficial dentures,  and  interstitial  gingivitis  of  local  and  constitutional 
origin. 

According  to  Kaufmann,  lacunar  absorption  is  the  most 
common  type.  This  may  be  true  in  morbid  anatomy  of  bone 
tissue  generally,  l)ut  it  is  not  true  of  absorption  of  the  alveolar 
process.  On  an  examination  of  hundreds  of  slides  prepared 
from  canine  and  human  jaws  (of  which  characteristic  types  are 
illustrated),  by  far  the  most  common  form  of  absorption  was 
found  to  be  halisteresis.  Perforating  canal  absorption,  which 
Kaufmann  has  "  occasionally  met  with,"  is  certainly  very  com- 
mon, while  lacunar  absorption  holds  third  posititm.  This  ordei' 
of  absorption  is  accounted  for  by  the  fact  that  where  struc-tures 


158  INTERSTITIAL    GINGIVITIS. 

are  transitory,  halisteresis,  as  quickest  method,  follows  by  the  law 
of  the  survival  of  the  fittest.  For  the  same  reason  perforating 
canal  absorption  should  stand  second.  The  blood  vessels  of  Von 
Ebner  being  most  numerous,  although  considered  smaller,  they 
would  naturally  be  the  second  tissue  involved.  As  in  interstitial 
gingivitis,  absoristion  of  the  alveolar  process  is  invariably  due  to 
inflammation,  halisteresis  apjDarently  starts  at  the  larger  Haver- 
sian canals  from  which  this  form  of  absorption  invariably 
originates. 

Interstitial  gingivitis  extends  to  the  alveolar  process  through 
the  periosteum  as  well  as  the  peridental  membrane  (not,  as  den- 
tists usually  believe,  by  way  of  the  peridental  membrane  alone). 
This  is  demonstrated  by  the  illustrations.  The  entire  alveolar 
process  thus  becomes  involved.  The  products  of  inflammation 
extend  through  the  Haversian  canals  (a  path  obviously  evident 
in  pathologic  illustrations),  setting  in  action  the  three  forms  of 
absorption  as  elsewhere  illustrated. 

Halisteresis  Ossium  («»/«?  of  salt,  trrs/ihu?  deprivation)  or 
decalcification,  is  that  process  of  absorj)tion  wherein  solution  of 
the  lime  salts  first  takes  ]3lace,  while  the  cartilage  or  matrix 
remains  for  the  time  undisturbed. 

Solution  of  the  lime  salts  begins  at  the  periphery  of  the 
Haversian  canal  and  advances  toward  the  center  of  the  tra- 
beculse.  This  absorption  follows,  as  a  rule,  the  bone  layers.  Bone 
centers  are,  therefore,  usually  the  last  to  be  absorbed.  Fre- 
quently decalcification  becomes  complete  ;  nothing  remaining  but 
the  organic  matrix  or  cartilage.  Finally,  this  is  also  entirely 
destroyed.  As  the  osteoblasts  occur  in  the  matrix  or  cartilage, 
it  is  not  difiicult  to  understand  that  absorption  may  extend  far, 
yet  restoration  of  the  alveolar  process  may  occur.  After  destruc- 
tion of  the  matrix  such  a  restoration  is  imjiossible.  New  fibrous 
tissue  may  be  partly  restored,  but  it  is  doubtful  if  the  alveolar 
process  can  be. 

Both  Ziegler'  and  Kaufmann-  divide  osteomalacia  into  senile 
and  juvenile.  The  latter  occurs  most  frequently  during  preg- 
nancy. In  senile  absorption,  after  a  certain  period,  the  entire 
skeleton  is  affected.     The  condition  begins  most  frequently  in 


'  Special  Pathological  Anatomy,  page  151. 
-Pathologische  Anatomie. 


conclusiojSts.  159 

the  "  vertebrae  and  thorax ;  hiter  extending  to  the  extremities." 
In  pregnancy  "  the  pelvic  bones  are  first  involved,  the  process 
then  extends  to  the  other  bones."  It  is  singular  that  the  alveolar 
process  should  have  been  so  much  neglected  by  pathologists, 
since,  in  both  states,  the  alveolar  process  becomes  involved  long 
before  the  bones  of  the  body. 

This  is  due  to  three  reasons :  first,  to  trophic  changes ;  sec- 
ond, to  the  alveolar  process?  being  a  transitory  structure ;  and 
third,  to  improj^er  care  of  the  gums  at  these  periods. 

Osteomalacia  occurs  in  the  alveolar  process  much  earlier  than 
at  the  so-called  "  senile  "  period.  It  is  found  at  twenty,  or  even 
earlier.  At  any  period  beyond  that  year,  it  occurs  probably  from 
the  prematurely  senile  states  of  which  precocity  is  a  type.  The 
lost  tissue  is  regained  often  after  confinement  in  the  "  preg- 
nancy "  type,  but  is  never  regained  in  the  senile. 

The  causes  which  produce  morbid  decalcification  are  not  thor- 
oughly determined.  Some  believe  it  to  be  due  to  lactic  acid  in 
the  system,  others  attribute  it  to  an  increased  amount  of  carbonic 
acid  in  the  blood.  Eisenhart  believes  it  to  be  due  to  a  want  of 
alkalinity  of  the  blood,  while  Von  Eechlirighausen  charges  it 
to  a  local  irritation  of  the  vascular  mechanism  of  the  bones.  It 
would  seem,  from  examinations  already  cited,  that,  so  far  as  the 
alveolar  process  is  concerned,  local  irritation  from  biochemic 
changes  in  the  blood,  as  suggested  by  Von  Rechlinghausen,  is 
the  chief  cause.  Premature  absorption  of  the  alveolar  process 
accompanies  the  movement  of  the  teeth  in  their  correction  or  in 
rapid  wedging.  Frequently  the  alveolar  process  is  never  fully 
restored,  thus  producing  a  predisposing  factor  for  future  disea^ie. 

Premature  absorption,  or  osteomalacia  of  the  alveolar  process, 
is  easily  recognized.  A  shrinking  of  the  gums  and  alveolar 
process  exposing  the  necks  of  the  teeth  is  very  conspicuous. 
Frequently  the  gums  and  mucous  membrane  covering  the  alveo- 
lar process  is  quite  red  (this  is  very  noticeable  in  dogs),  and  a 
thinning  of  the  alveolar  process  over  and  between  the  roots  of 
the  teeth.  The  process  of  one  tooth  only  may  become  involved ; 
again  the  process  over  two,  or  the  whole  jaw,  and  again  both  jaws 
become  affected. 

When  osteomalacia  occurs,  either  of  pregnancy  or  senile 
type,  although  the  tissues  be  seemingly  restored  to  iR'ulth,  struc- 


160 


INTEEl^TITIAL    GINGIVITIS. 


tural   change  has  taken   phice  to  such  an  extent  that  it  ever 
remains  a  predisiaosing  factor  to  interstitial  gingivitis. 

In  Fig.  36  may  be  seen  the  bhwd  vessels  of  Von  Ebner. 
These  blood  vessels  are  also  to  be  observed  in  Fig.  55.  They 
are  very  common  in  the  alveolar  process  and,  according  to  Volk- 
mann,  are  the  source  of  the  perforating  canals  which  bear  his 
name. 


X60.     ;i-incliobj.    No.  Oc. 

Fig.  66. —  Cnoss  Section  of  Tooth,  Alveolar  Process  and  Peridextal  Mejebrane, 
Showing  Lacunar  Arsorptiox.    Man. 


C,  C'ementum.        D,  Dentine.        I,  Peridental  Membrane. 
O,  Lacunar  Alssorption. 


J,  Alveolar  Process. 


These  canals  run  in  all  directions.  After  absorption  has  gone 
on  to  form  medullary  spaces,  these  canals  penetrate  through  the 
trabeculse  from  one  sj)ace  to  the  other  (Fig.  38).  The  position  of 
this  type  of  absori^tion  in  the  order  of  fre(piency  comes  from  the 
fact   that,  in  this   disease,  absorption   is  almost  entirely  due  to 


('()X('Lrsi().\> 


161 


inflaniination  ;  licncv  the  hlood  A'eissel.s  arc  the  iirst  to  liccoinc 
involved.  Those  entering  the  Haversian  canals,  heing  the  larger, 
are  first  affected,  and  hence  halisteresis  naturally  precedes. 

When  irritation  takes  place  in  a  nerve  or  part  of  bone  which 
is  about  to  be  absorbed,  nuiltinuclear  cells  arise  at  the  border  in 
the  2Jei"iosteuni  and  peridental  mend)rane.  They  attach  them- 
selves to  the  surface  of  the  bony  trabeculie.  According  to  Sud- 
ilutli,  "  the  absorber  and  the  absorl)ed  must  be  in  touch  with  each 


X  300.    No.  i.  projection  ocular.    D.  D.  obj.    Zeiss. 
Fig.  67. — Section  of  Peridental  Membrane,  Showing  Lacunar  Absorption  in  Dog. 
.1,  Alveolar  Process.    O,  Lacunar  Absorption.     I',  Inflamed  Peridental  IMenibrane. 

other."  Kollikcr  has  named  thvsv  cells  "Osteoclasts,"  which 
tei'iu  has  come  into  general  use.  Very  soon  after  these  cells 
make  theii-  appearance,  cavities  ai-e  seen  in  the  bone  tissue. 
These  cavities  are  called  Howshi])"s  laciune.  Lacunar  al)s()rp- 
tion,  as  elsewhere  sliOAvn,  takes  place  as  a  result  of  irritation  and 
overstimulation.     Fio-.  6(5  shows  a  cross  section  of  the  end  of  one 


162  INTERSTITIAL    GINGIVITIS. 

of  the  buccal  roots  of  Fig.  68.  As  will  be  observed,  this  tooth 
was  held  in  place  by  two  buccal  roots.  As  much  resistance  was 
required  of  these  two  roots  as  was  formerly  required  of  three. 
Irritation  due  to  excessive  force  in  mastication  was  causing 
absorption.  Round-cell  inflammation  is  not  present  in  the  peri- 
dental membrane.  The  irritation  may  be  continued  until  inflam- 
mation sets  in  and  until  the  bone  is  entirely  absorbed,  as  noticed 
in  Fig.  67.  Small  round-cell  inflammation  is  quite  noticeable  in 
the  surrounding  tissue. 

Sometimes  these  lacunae  may  be  seen  extending  along  the 
entire  length  of  bone.  As  many  as  thirty-seven  may  be  counted 
in  some  fields  (Fig.  37).  Lacunar  absorption  frequently  so 
extends  through  the  Haversian  canals  as  to  cut  off  pieces  of  the 
alveolar  process.  A  casual  glance  at  Fig.  66  demonstrates  this. 
This  figure  could  be  multiplied  many  times  from  other  slides. 
These  frequently  come  away  with  the  peridental  membrane  when 
the  tooth  is  extracted.  This  is  often  noticed  in  removing  loose 
teeth  chie  to  interstitial  gingivitis.  By  passing  the  finger  over 
the  surface  of  the  root,  the  rough  pieces  of  bone  may  be  easily 
felt. 

Aside  from  the  forms  of  absorption  already  noted,  absorption 
of  the  alveolar  process  is  often  seen,  the  result  of  neuropathic 
lesions.  Paretic  dementia,  diseases  of  the  spinal  cord,  low  forms  of 
inflammation,  general  debility  and  traumatism,  together  with 
unhygienic  conditions  of  the  mouth,  are  fruitful  sources  of  inter- 
stitial gingivitis  and  absorption  of  the  alveolar  2:)T0cess.  Absorp- 
tion of  the  alveolar  process  takes  place  also  in  diathetic  diseases 
in  which  the  nervous  system  has  been  involved  (syj)hilis,  scurvy, 
lithsemia,  etc.). 

PYOKKHCEA    ALVEOLARIS    FROM    INTERSTITIAL    GINGIVITIS. 

Recovery  from  interstitial  gingivitis  and  return  to  normal 
conditions  without  change  in  structure  is  called  restoration. 
Should  the  damage  be  extensive,  and  accumulations  of  cell  and 
liquid  exudate  so  press  upon  the  tissues  as  to  extinguish  their 
vitality,  ordinary  restoration  is  impossible.  This  is  also  true 
when  the  inflammation  is  more  decided  and  persistent.  This 
inflammation  may  extend  throughout  the  tissue.  Absorption  of 
the  alveolar  process  may  take  place,  and  exfoliation  of  the  teeth 


CONCLUSIONS.  163 

result  without  jius  infection.  The  tissues  may  be  in  a  favorable 
condition  for  infection,  yet  the  mouth  and  blood  vessels  be  free 
from  pus  germs.  This  is  not  uncommon.  The  tissues  are  often 
invaded,  however,  by  micro-organisms,  resulting  in  suppuration. 
Interstitial  gingivitis,  with,  pus  infection  in  and  about  the  alveolar 
process,  resembles  suppuration  elsewhere  in  the  body.  It  results 
either  in  an  abscess  or  ulceration.  An  abscess  is  a  collection  of 
pus  within  the  tissues.  Ulceration  is  a  collection  of  pus  upon 
the  surface  of  the  tissues.  Both  of  these  marked  conditions, 
being  dependent  upon  intlammation,  are  associated  with  intersti- 
tial gingivitis. 

Suppuration  (due  to  jiyogenic  cocci)  is  the  usual  termination 
of  infective  inflammation.  Healthy  gum  tissue  is  intolerant  of 
bacteria,  and  will  resist  the  invasion  of  micro-organism.  When 
inflammation  takes  place,  the  diseased  part  is  unable  to  resist 
them.  Lowered  vitality  of  tissue  is  a  fruitful  source  of  infection 
and  supj^uration.  Since,  as  Miller'  has  shown,  pus  germs  are 
found  in  almost  every  mouth,  infection  is  a  very  probable  outcome 
of  gingivitis. 

The  organism  most  frequently  producing  pus  are  the  staphy- 
lococcus pyogenes  aureus,  and  albus.  These  have  a  tendency  to 
accumulate  in  groups.  When  they  collect  at  a  given  point  in  the 
tissue,  suppuration  results.  The  streptococci  (occasionally  pres- 
ent in  the  mouth)  do  not  as  a  rule  produce  local  suppuration,  but 
sjDread  through  the  tissue  by  way  of  the  lymphatics  and  blood 
vessels,  and  eventually  give  rise  to  abscess.  The  delicate  reticu- 
lum of  the  blood  vessels  found  in  the  Haversian  canals  is  a 
convenient  lodging  place  for  swarms  of  bacteria,  OAving  to  the 
slowness  of  the  blood  current  and  the  tortuous  course  of  the 
blood  channels.  When  ~  the  circulation  has  been  imj^eded  or 
arrested  by  an  extravasation  of  blood  or  congestion  of  a  part,  the 
conditions  are  favorable  for  intravascular  infection  if  organism 
happen  to  be  circulating  in  the  blood  at  the  time.  As  we  have 
seen,  micro-organisms  may  from  time  to  time  be  found  in  the  cir- 
culation, particularly  in  individuals  of  feeble  constitution.  The 
anatomic  nature  of  the  part  will  therefore  determine  suppuration 
in  certain  localities. 


'  Micro-Orgaiiisms  of  the  Human  Mouth. 
-  American  Text-Book  of  Surgery. 


164  IXTEESTITIAL    GIXGIVITIS. 

Ill  whatever  part  or  tissue  the  change  may  occur,  the  j)rocess 
is  the  same.  The  original  structures  disintegrate.  Their  place 
is  taken  hy  a  closely  packed  crowd  of  migrated  leucocytes. 
Should  the  cause  continue  to  act,  the  process  culminates  in  the 
formation  of  pus.  The  migrated  cells  cut  off  from  proper 
nutrition  by  pressure  are  exposed  to  the  injurious  action  of 
micro-organism.  The  central  cells  of  the  group  degenerate  from 
want  of  nutrition  or  die  from  direct  action  of  the  irritation.  The 
intercellular  substance  softens,  and  the  liquid  exudate  from  the 
surrounding  parts  mingles  with  the  broken-down  tissue  to  form 
an  abscess. 

As  I  have  shown,  foci  of  infection  and  intense  inflammation, 
to  the  point  of  degeneration  and  liquefaction,  occur  in  most 
every  locality  within  the  peridental  membrane,  jieriosteum  and 
alveolar  ^^I'ocess.  These  abscesses  are  just  as  likely  to  j^oint 
upon  the  surface  of  the  gum  as  on  the  inner  surface  next  to  the 
root  of  the  tooth.  When  abscesses  form  in  and  about  the 
alveolar  process,  with  fistulas  oj^ening  outside  of  the  inner 
alveolar  wall,  the  disease  cannot  be  entitled  pyorrhoea  alveolaris, 
since,  as  elsewhere  shown,  strict  definition  of  this  title  implies 
pus  flowing  from  the  alveolus. 

Abscesses  which  discharge  their  contents  into  the  space 
between  the  alveolar  wall  and  the  root  of  the  tooth,  and  ulcer- 
ation of  the  peridental  membrane  only,  could  literally  be  con- 
sidered under  the  head  of  pyorrhoea  alveolaris. 

Abscesses  in  and  about  the  alveolar  process  (other  than  those 
due  to  dead  pulps)  are  very  common.  This  is  due  first  to  the 
unstable  conclition  of  the  structures,  and  second  to  the  ready 
access  of  ]3us  germs  through  the  inflamed  gums  and  peridental 
membrane.  Those  most  susceptible  to  infection  are  patients  who 
are  anaemic  and  below  par  in  vitality,  and  whose  gums  have 
become  inflamed  either  from  local  or  constitutional  causes. 
Especially  is  this  the  case  in  those  who  have  osteomalacia 
where  the  gums  have  receded  quite  a  distance  from  the  necks 
of  the  teeth.  Pus  germs  collect  at  the  necks  of  the  teeth,  infect 
the  raw  inflamed  surfaces  of  the  epithelial  layer,  and  entering 
the  circulation  are  carried  into  the  deeper  structures.  Intense 
inflammation  results.  Abscesses  form,  discharging  their  con- 
tents upon  the  surface.  Pus  germs  also  enter  the  deeper  struc- 
tures through  exposed  pulps. 


(■()N(']j'Si()Xs.  165 

Two  cases  of  interest  in  tliis  eoiineetion  occurred  recently  in 
practice.  An  active  Inisiness  man,  fit'ty-tive  yeai's  of  age,  |>re- 
seuteil  himself  Avith  an  abscess  over  the  buccal  roots  of  the  left 
superior  second  molar.  There  were  no  dead  pulj^s  in  any  of  the 
teeth  u])ou  that  side  of  the  jaw.  Absorption  of  the  alveolar 
process  and  contraction  of  the  gums  had  occurred  around  all  the 
teeth.  He  had  been  overworked  and  was  nervously  exhausted. 
Five  years  ago  cataracts  were  removed  from  both  eyes.  He  is 
exceedingly  sensitive  to  pain.  Examination  of  blood  rcs-ealed 
slight  angemia.  On  examination  of  urine,  other  than  a  specific 
gravity  of  1028,  it  was  found  normal.  The  abscess  was  lanced 
and  cavity  cleansed.  It  healed  within  a  week.  8ul)sequently 
he  returned  Avith  anothei-  abscess  over  the  root  of  the  right 
superior  central  incisor.  Live  jjulps  Avere  in  all  tlie  teeth  tipon 
this  side  as  far  as  the  second  molar.  Infection,  therefore,  must 
have  occurred  through  the  gnm  and  peridental  membrane. 

The  teeth  of  a  lady  forty-six  years  of  age  were  being  j^ut  in 
order ;  after  filling  a  cavity,  May  14,  1899,  she  called  attention 
to  a  space  between  the  second  and  third  supei'ior  right  molars, 
and  stated  food  lodged  at  that  point,  causing  pain  and  bleeding. 
The  space  Avas  cleansed  Avitli  an  excavator  and  the  cavity 
syringed  Avith  Avarm  Avater  and  then  explored.  Absorption  of 
the  gums  and  alveolar  process  had  extended  one-half  the  length 
of  the  buccal  root.  Applications  of  iodin  Avere  made  to  reduce 
the  inflammation.  The  patient  Avas  dismissetl  Avith  an  appoint- 
ment for  May  17.  She  returned  at  the  appointed  time  Avith  an 
abscess  over  the  palatine  root  as  large  as  the  thumb.  The  lady 
had  had  acute  i^ain  from  the  time  she  left  the  oflice  until  her 
return.  The  parts  had  been  infected  with  i^us  germs  through 
the  peridental  membi-ane.  The  pus  Avas  collected  in  a  tin  tea 
spoon,  from  which  cultures  Avere  obtained  and  glass  slalts 
smeared  for  microscojiic  examination.  The  pus  was  examined 
by  George  T.  Carjienter  for  calcic  deposits ;  the  usual  asejitic 
l)recautions  having  been  taken. 

Microscopic  examination  revealed  the  usual  pus  geiins. 
Chemical  analysis  for  calcic  deposits  in  the  pus  Avas  made  as 
folloAVS  :  The  pus  Avas  placed  in  a  test  tulie  with  hydrochloric 
acid  (diluted  Avith  four  times  its  bulk  in  Avater).  The  phosphate 
is  dissolved.      It  is  then   diluted  with  Avatei',  boiled,  and   when 


160  INTEESTITIAL    GINGIVITIS. 

cold  excess  of  solution  of  ammonia  added.  The  lime  salts  are 
then  re-precipitated  as  an  amorphous  j)Owder. 

Many  dentists,  ignoring  the  laws  of  pathology,  insist  that 
intense  inflammation  in  remote  parts  of  the  alveolar  process  is 
not  due  to  invasion  by  micro-organisms  of  an  inflamed  tissue, 
but  is  the  result  of  gouty  deposits.  The  utter  lack  of  foun- 
dation for  this  theory  must  be  apparent  on  the  slightest  study 
of  pathology. 

Ulceration  is  always  located  ujDon  the  surface  of  a  tissue. 
When  ulceration  occurs  from  contact  irritation  of  the  gum  margin 
or  by  mechanical  or  chemical  means,  congestion  and  oedema 
result,  thickening  of  the  epithelial  layer  and  increased  growth  of 
cells.  The  sub-epithelial  tissue  becomes  inflamed.  The  process 
is  not  unlike  that  of  the  formation  of  an  abscess,  since  the 
infected  tissue  resembles  part  of  an  abscess  wall.  In  slowness  of 
progress  only  does  ulceration  differ  from  acute  inflannnation. 

Such  is  the  condition  of  the  peridental  membrane.  When 
simple  gingivitis  becomes  chronic,  the  inflammation  extends  to 
the  surface  of  the  peridental  membrane.  This  is  situated  at  the 
lower  extremity  of  a  cul-de-sac,  formed  by  the  gum  on  the  one 
hand  and  the  tooth  on  the  other.  This  cavity  is  fllled  with 
foreign  material  in  which  decomposition  continually  occurs. 
The  tissues  are  thereby  constantly  irritated.  Necrosis  occurs  at 
the  surface.  In  the  deeper  tissues  that  have  become  inflamed 
pus  cells  also  are  found.  These  not  only  arise  from  the  normal 
blood  vessels  in  the  vicinity,  but  also  from  the  granulation  tissue. 
The  causes  of  peridental  membrane  ulceration  are  disturbances  of 
nutrition,  endarteritis  obliterans  (a  disease  of  the  blood  vessels 
due  to  constitutional  diseases,  such  as  syphilis,  scurvy,  tubercu- 
losis, uric  acid  and  other  blood  poisons)  and  starvation  of  tissue, 
feeble  circulation  (as  in  anaemia)  and  inflammation.  If  the 
ulcerated  surface  be  examined  under  the  microscope,  a  general 
thickening  of  the  tissues  will  be  seen.  In  the  papillary  layer 
deposits  of  blood  pigment  (Fig.  52)  occur.  The  surface  is 
covered  with  granulation  tissue.  The  tissue  may,  in  part, 
resemble  the  tj-pe  of  healthy  granulation.  It  is  composed  of 
round  cells  closely  packed  together  and  supplied  with  rich  capil- 
lary network.  Coagulation  necrosis  from  breaking  down  of 
granulation  tissue  may  be  present. 


CONCLUSIOXS.  1<>7 

CONSTITUTIONAL    EFFECTS    OF    J'YOHIUKEA    A  I.VKOl-AKI.S. 

The  influence  of"  the  staine  of  interstitial  iiiiigivitis  known  as 
pyorrhoea  alveolaris  on  the  system  has  been  (Hsenssed  hy  .lolni 
Fitzgerald.'  He  points  out  that  pj^orrlnjea  alveolaris  may  act  in 
three  different  ways  in  the  causation  of  systemic  disease.  The 
pus,  with  its  multitude  of  putrefactive  organisms  and  decayed 
food  remnants  from  the  pus  pockets,  may  be  swallowed  and  either 
act  locally  upon  tlic  stomach  Avail  or  set  up  fermentation  of  the 
stomach  contents.  The  toxins  generated  in  the  mouth  may  be 
absorbed  by  the  nnicous  membrane  of  the  mouth  or  stomach  and 
thus  pass  into  the  general  circulation.  The  local  conditions  of 
the  mouth  may  favor  the  growth  of  pathogenic  organisms,  and 
thus  render  the  patient  more  liable  to  certain  infectious  disorders, 
noticeably  influenza.  The  power  of  pyorrhoea  alveolaris  to  pro- 
duce aggravation  of  existing  gastric  trouble  reaches  its  maxinuim 
in  cases  where  there  is  retention  of  food  residues.  This  happens 
when  the  muscular  walls  of  the  stomach  are  in  a  state  of  atony 
and  also  when  there  is  some  pyloric  obstruction  which  prevents 
the  organ  emptying  itself.  In  both  these  conditions  stomach 
dilatation  is  eventually  produced,  with  the  result  that  the  stomach 
is  never  completely  emptied.  The  first  condition  is  a  very  fre- 
quent concomitant  of  neurasthenia  and  allied  .states.  It  is  easy 
to  see  how  pyorrhoea  can  at  once  be  23redisposed  to  by  neuras- 
thenic states  and  at  the  same  time  increase  the  neurasthenia  by 
causing  gastric  trouble  through  its  interference  with  gastro-intes- 
tinal  digestion  under  the  conditions  mentioned. 

Herschell~is  of  opinion  that  nuniy  of  the  chronic  indigestions 
are  due  to  continual  absorjition  of  pus  into  the  system  from  a 
pyorrhoea  alveolaris.  In  these  cases  he  remarks  there  should  be 
other  evidences  of  the  absorption  of  toxins,  such  as  pigment  sjiots, 
urticaria,  etc.  Fitzgerald  points  out  that  the  bacterium  coli  com- 
mune is  a  constant  inhabitant  of  the  oral  cavity,  and.  as  a  I'ule, 
seemingly  harmless.  Under  the  influences  of  a  culture  medium 
such  as  would  be  furnished  by  a  pyorrhoea  or  an  inHammatory 
state  of  the  gum,  this  bacterium  might,  as  elsewhere  in  the 
mucous  membrane,  acquire  sufficient  virulence  to  produce  serious 
disturbances  of  the  system,  such  as  colitis,  dysentery  and  cholera 
nostras. 


'  Clinical  Journal,  March  (i,  1899.  '-'  Indigentinn,  1.S9-") 

12 


168 


IXTEESTITIAL    GINGIVITIS. 


CALCIC    DEPOSITS. 

There  are  many  instances  in  which  interstitial  gingivitis  takes 
place,  with  absorption  of  the  alveolar  process  and  exfoliation  of 
the  teeth,  Avithont  calcic  deposits.  In  such  cases  the  blood  is 
charged  with  only  sufficient  lime  salts  for  the  nourishment  of  the 
body.  The  waste  products  are  carried  off  with  the  excreta.  In 
absorption  of  the  alveolar  process,  inflammation  does  not  seem  to 
extend  to  the  capillaries,  the  result  of  which  is,  this  waste  mate- 
rial is  carried  into  the  circulation.     In  this  way,  calcic  material 


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does  not  collect  in  the  fluids  and  upon  the  teeth.  In  those  cases 
in  which  pus  is  not  present  (there  being  a  lessened  amount  of 
carbonic  acid)  calcic  deposits  rarely  take  place.  The  percentage 
of  teeth  so  found,  however,  is  not  so  large  as  those  with  deposits. 
Examination,  by  a  magnifying  glass,  of  a  recently  extracted 
tooth  (whose  root  is  covered  with  serumal  deposits)  shows  the 
lime  deposited  in  a  manner  resembling  that  of  stalactite  forma- 
tion. The  deposits  often  stand  out  distinctly  independent  of  each 
other  (Fig.  68).  This  condition  is  due  to  deposits  from  the  blood, 
resultant  on  biochemic  chauaes  in  the  inflamed  tissues.     Blood 


COXCLUSTONS. 


160 


stasis  occurs  in  the  gum  tissue,  fibrous  tissue  of  the  periosteum, 
peridental  membrane  and  alveohir  process,  througli  whirl)  last 
nuwh  of  the  blood  circulates.  This  stasis  may  be  consequent 
upon  conditions  varying  from  simple  inflammation  to  disease  of 
the  endothelium,  producing  endarteritis  obliterans. 

The  blood  has  become  surcharged  in  all  constitutional  dis- 
eases, but  more  especially  in  kidney  lesions.  Deposits  occur  in 
the  fluids  and  upon  the  roots  of  the  teeth.  Frequently  the 
deposit  is  found  only  on  one  side  or  only  at  one  particular  spot 
on  the  side  of  the  root;  again  at  the  apex,  when  the  pulp  is 
destroyed.  It  may  encircle  the  root.  The  inflammatory  process 
may  therefore  be  circumscribed  as  to  area  or  the  whole  tissue 
may  be  involved.  The  deposit  is  circumscribed  in  the  area  of 
inflammation.  The  calcareous  matter  absorbed  from  the  alveolar 
process  in  the  immediate  vicinity  of  the  root  is  not  improbaljly 
soon  deposited  upon  the  root  or  roots  because  of  the  impeded  cir- 
culation.' "  Ossification,  as  has  been  well  remarked,  is  an  active 
development  in  which  the  tissues  are  abundantly  supplied  with 
blood.  There  is  a  rapid  cell  proliferation,  and  the  calcareous 
matter  forms  an  intimate  and  permanent  union  with  the  tissues. 
Calcification,  on  the  other  hand,  is  passive,  and  indicates  an 
impaired  vitality.  Calcification  begins  as  a  rule  in  the  intersti- 
tial tissue.  In  regard  to  the  origin  of  the  calcareous  salts,  it  is 
generally  believed  that  they  come  more  or  less  immediately  from 
the  blood,  although  Rokitansky  supposes  that  they  Avere  foi-mcd 
by  a  metamorphosis  of  the  tissues  involved." 

Calcification  is  due  to  two  varieties  of  causes:  general  and 
local.  The  former  are  dependent  upon  changes  in  the  blood  or 
its  circulation,  due,  for  exam^^le,  to  disease  or  senile  change.  In 
composition  the  blood  may  be  so  altered  as  to  contain  an  abnormal 
amount  of  calcareous  matter.  This  effect  is  most  commonly  pro- 
duced by  absorption  of  lime  salts  from  osseous  tissues  which  are 
the  seat  of  extensive  caries,  osseous  cancer,  osteo-sarcoma  or  osteo- 
malacia. The  calcareous  matter  thus  taken  up  is  conveyed  to 
other  and  often  remote  parts  and  there  deposited,  constituting  the 
"metastatic  calcification"  of  Virchow.  Kuttner,  of  St.  Peters- 
burg, has  observeil  a  rapid  calcification  of  nearly  all  of  the  smnll 
arteries  as  a   result    of  cai'ies  involving  the   dorsal   and   luiubar 

'  Wood's  Handbook  of  Medical  Sciences,  Vol.  I,  page  743. 


170  INTERSTITIAL    GINGIVITIS. 

vertebrae  in  a  niueteen-year-old  boy.  Virehow  has  observed  & 
case  in  which,  as  a  result  of  bone  cancer  (aifecting  nearly  all  of 
the  larger  bones,  particularly  the  borders  of  the  vertebrae  and  the 
skull),  the  calix  and  pelvis  of  the  kidneys,  the  lungs,  parenchyma, 
and  the  stomach  mucous  membrane  were  calcified. 

Circulation  of  the  blood  may  be  retarded  and  thus  favor  pre- 
cipitation of  calcareous  matter  normally  held  in  solution.  To  this 
is  chiefly  due  the  frequency  of  calcareous  degeneration  from 
general  loss  of  vitality. 

Calcification  rarely,  if  ever,  depends  upon  general  causes 
alone.  There  is,  as  a  rule,  a  local  influence.  Very  often  this  is 
due  to  preexisting  chronic  inflammation.  Old  accumulations  of 
pus  and  exudates  are  exceedingly  prone  to  calcification.  The 
deposit  frequently  occurs  also  in  fibrous  walls  surrounding  the 
accumulation.  A  mere  loss  of  function  ^predisposes  to  calcification. 
Such  is  the  case  in  and  about  the  tissue  of  the  alveolar  process. 
The  decalcified  material  from  the  alveolar  process  collects  in  the 
soft  tissues  as  well  as  upon  the  roots.  In  his  pajjer  George  T. 
Carpenter '  asks  the  question  :  Can  a  tissue  be  absorbed  and  still 
remain  as  debris  in  the  pocket?  Such  is  the  condition  found, 
and  this  can  be  easily  proven.  Take  the  contents  of  a  pocket 
and  dissolve  it  in  hydrochloric  acid,  add  three  times  its  bulk  of 
water,  to  this  add  ammonia,  which  will  j^recipitate  the  phosphate 
and  the  calcium.  The  same  results  may  be  obtained  by  rinsing 
a  freshly  extracted  tooth  of  a  pyorrhoea  case  in  cold  water. 
With  a  stiff"  brush  remove  the  accumulation  and  place  it  in  a 
test  tube,  add  hydrochloric  acid  and  more  water  if  necessary. 
To  this  add  a  solution  of  ammonia  and  the  lime  salts  are  precipi- 
tated. 

Roots  of  teeth  that  have  become  entirely  denuded  of  peri- 
dental membrane  and  bathed  in  pus  accumulate  large  quantities 
of  calcic  dejiosits  direct  from  the  absorption  of  the  alveolar 
process. 

Difference  of  opinion  exists  as  to  the  nature  of  the  process 
immediately  involved  in  j)recipitation  of  lime  salts.  The  simplest 
and  seemingly  most  logical  exjjlanation  is  that  the  process  is 
similar  to  that  involved  in  the  formation  of  stalactites.    A  certain 


'  Some  Points  on  the  Etiology,  Patiiology  and  Treatment  of  Persistent  Pyorrhoja 
Alveolaris, 


CONCLUSIONS.  171 

amount  of  ealearcoiis  matter  is  a  normal  constituent  of  the  blood. 
Herein  it  is  held  in  solution  l)y  t'arl)onic  acid,  always  present  in 
sufficient  quantity  for  this  jjurpose.  When  the  circulation  is 
impeded  the  free  carbonic  acid  (because  of  its  great  diflf'usil)ility) 
is  readily  absorbed  by  the  tissues  or  goes  to  form  new  compounds, 
necessitating  a  precipitation  of  the  calcareous  matter.  Calcareous 
matter  may  be  deposited  in  either  a  fibrous  or  fluid  matrix.  It 
shows  a  preference  for  newly  formed  fibrous  tissue,  particularly 
when  this  is  associated  with  old  tissue  undergoing  fatty  degenera- 
tion and  absorption.  In  a  fil)rous  matrix  the  infiltration  usually 
begins  in  the  intercellular  substance,  but  may  involve  the  cellular 
elements  at  a  later  period.  In  a  fluid  matrix  (like  pus)  the 
,  granules  are  frequently  deposited  primarily  within  the  cells.  The 
process  may  advance  slowly  or  rapidly.  AVhen  local  causes  exert 
the  chief  influence  it  is  more  limited  in  area  of  invasion  than 
when  there  is  a  general  factor  in  its  jiroduction,  as  in  the  meta- 
static forms. 


CHAPTER  XVI. 

TREATMENT. 

The  clinical  history  of  interstitial  gingivitis  is  essentially  that 
of  any  other  disease  of  the  mneons  membranes.  The  disorder 
responds  qnickly  to  treatment  at  its  outset.  Later,  its  complica- 
tions and  the  extent  of  structure  involved  render  treatment  very 
ineffiacious,  and  always  insure  loss  of  the  tooth.  As  the  general 
surgeon's  duty  is  to  save  life,  if  need  be,  at  the  expense  of  limb, 
or  organ,  but  to  save  these  last  if  possible,  so  the  dental  surgeon's 
duty  is  to  remove  the  teeth,  if  need  be,  for  the  benefit  of  the 
general  health,  but  to  save  them,  when  possible,  for  the  same 
reason.  The  patient,  therefore,  should  be  told  frankly  at  the 
outset  of  interstitial  gingivitis,  that  it  is  a  condition  requiring 
time  for  its  treatment,  and  should  not  be  given  that  prognosis 
too  frequently  made  of  quick  cure.  To  such  a  prognosis  many 
a  case  of  constitutional  disorder  is  due.  The  dentist  is  a  practi- 
tioner of  a  surgical  specialty,  not  a  mere  tooth-puller.  The  sur- 
gical side  of  dentistry  has  received  too  much  attention,  however  ; 
the  medical  or  prophylactic  too  little.  Patients  are  beginning  to 
jiay  more  attention  to  the  prophylaxis  of  the  teeth  and  jaws,  and 
need  but  little  encouragement  and  instruction  to  see  the  absolute 
necessity  of  early  prophylaxis  and  treatment  of  interstitial  gin- 
givitis. The  trend  in  general  medicine  is  to  j^rophylaxis,  and 
this  has  undoubtedly  so  imj^ressed  patients  as  to  open  the  way 
for  dental  prophylactic  suggestions.  Viewing  the  question  from 
the  narroAvest  standpoint  of  remuneration,  the  dentist  could  not 
fail  to  profit  by  instructions  to  his  patients  on  j^ro^ihylaxis.  He 
certainly  fails  in  his  duty  as  the  member  of  a  learned  profession 
by  not  doing  this.  Furthermore,  with  the  known  necessity  for 
proj)hylaxis,  it  is  an  open  question  whether  the  failure  to  inform 
the  patient  of  the  dangers  of  the  incipient  disease  could  not  be 
successfully  pleaded  as  a  basis  for  a  malpractice  suit. 

From  the  etiology  of  this  disease,  the  treatment  would  ajjpear 
simple  and  easy. 


TREATMENT.  173 

Early  diagnosis  is  not  difficult,  since  the  sini])le  infliunniation 
of  the  gums  is  easily  recognized  by  the  patient.  Bk'cding  when 
the  toothbrush  or  tootlipick  is  used  can  never  be  mistaken. 
The  dentist  with  liis  accomplished  eye  can  readily  detect  the 
slightest  change  in  color  or  puffiness  around  the  necks  of  the 
teeth  or  of  the  festoons  between  the  teeth.  Redness,  puffiuess 
and  bleeding  are  pathognomonic  of  this  disease  in  its  incip- 
iency. 

Few  dentists  have,  however,  given  this  stage  of  the  disease 
any  thought,  albeit  they  have  filled  the  teeth  of  their  patients 
from  year  to  year.  I  have  in  mind  three  patients  with  loose 
teeth  and  inflannnaticjn  extending  throughout  the  peridental 
membrane  and  alveolar  process,  who  had  been  under  an  old 
practitioner  now  retired  from  practice.  The  patients  had  never 
had  the  gums  treated  or  even  their  teeth  cleaned.  This  is  not 
an  uncommon  occurrence.  The  excuse  usually  made  by  the 
dentist  is  that  he  cannot  get  paid  for  his  time.  Gingivitis  is 
a  disease  which  the  dentist  is  as  much  bound  to  treat  and  cure 
as  any  disease  of  the  mouth  and  teeth.  It  is  a  part  of  his 
specialty  which  should  not  be  ignored.  It  is  claimed  that  the 
dental  profession  is  overcrowded.  Were  this  disease  treated 
until  the  gums  were  placed  in  a  healthy  condition,  there  would 
be  practice  enough  for  as  many  more  dentists  as  there  are  today. 
The  busy  dentist  of  today  could  attend  only  to  one-half  the 
patients  w4iom  he  now  serves. 

The  treatment,  then,  should  be  proi^hylactic  in  its  nature, 
preventive  rather  than  corrective.  The  disease  and  treatment 
is  not  unlike  an  inverted  pyramid  :  the  farther  from  the  apex  or 
beginning,  the  more  difficult  and  hopeless  the  task  becomes. 
Since  the  teeth  have  nothing  directly  to  do  with  this  disease, 
they  should  be  ignored.  In  the  early  stages,  the  gums  should 
receive  proper  attention.  These,  like  other  parts  and  organs  of 
the  body,  must  be  exercised  to  be  kept  healthy.  The  gums 
should  be  properly  massaged,  just  as  the  liver,  kidneys  or  skin 
are  when  they  are  not  doing  proper  work.  This  can  be  accom- 
plished by  properly  made  brushes.  The  ordinary  toothbrush  is 
not  adapted  to  the  work  under  discussion.  It  will  brush  the 
teeth  but  not  reach  the  gums.  What  is  needed  is  a  massage 
bi'usli  tliat  will  miss  tiic  tcclli  to  a  certain  extent,  but  will  reach 


174  INTERSTITIAL    GINGIVITIS. 

the  gums  and  contract  them  tight  around  the  teeth,  thus  pre- 
venting the  accumulation  of  foreign  substances.  The  jjatient 
should  be  instructed  with  this  single  idea  in  view,  "that  the 
gum  margin  is  to  be  exercised  and  stimulated  and  not  the  teeth, 
which  must  be  ignored."  A  brush,  properly  made  for  gum 
massage  (Fig.  69),  will  do  sufficient  work  upon  the  teeth  with 
the  aid  of  the  floss  silk  and  toothpick.  It  should  have  printed 
upon  the  handle,  in  large  letters,  "gum  massage  brush."  The 
handle  should  be  bent  a  little  more  than  the  "  prophylactic,"  so 
that  the  end  containing  the  bristles  can  be  brought  in  contact 
with  the  gum,  posterior  to  the  central  incisors,  upper  and  lower, 
and  around  the  third  molar  teeth.  There  should  be  a  tuft  of 
bristles  at  the  point  with  a  space  for  the  teeth.  The  tuft  should 
be  longer  than  those  on  the  body  of  the  brush.     This  tuft  will 


reach  the  gums  at  all  points  inside  of  the  mouth  and  around 
the  molars.  The  bristles  on  the  body  must  have  sj)aces  between 
them,  so  that  when  the  upward  and  downward  movement  is 
given,  the  bristles  will  go  between  the  teeth  and  reach  the  gum 
festoons.  The  bristles  must  be  medium  and  hard.  The  quality 
of  bristles  must  de]Dend,  however,  upon  the  condition  of  the 
gums.  If  they  be  soft  and  spongy,  the  medium  may  be  used. 
If  the  processes  are  heavy  and  thick,  the  gums  swollen  and 
engorged  with  blood,  hard  bristles  must  be  used.  Soft  bristles 
(although  sometimes  recommended)  should  never  be  used. 

The  antique  theory  that  vigorous  stimulation  is  injurious  is 
too  much  accepted.  Barrett,'  for  example,  says,  "massage  of  the 
gums  with  the  ball  of  the  finger  and  by  the  frequent  use  of  a 
rather  soft  brush  should  be  resorted  to."  Beodecker "  remarks 
that  too  frequent  application  of  the  toothljrush  is  sufl!icient  to 

1  Dental  Cosmos,  188.3,  page  5.32. 

-Anatomy  and  Patholog)'  of  the  Teetli,  page  l!()5. 


TnRAT:\rENT.  175 

prdiliu'c  |):i])illiiry  liy]i('i'|)lasi!i.  Tomes'  Hays,  "  in  my  (iwii  cxpt'- 
riciu'c  1  havr  tuiiiid  tliat  frequent  and  vigorous  rubbing  of  the 
gums  with  tlie  finger,  sluuupooiug  them  in  fact,  has  often  been 
productive  of  great  advantage,  the  patient  of  course  lieing  cau- 
tioned not  to  rub  the  actual  edge ;  but  even  on  this  point  there 
is  difference  of  opinion,  for  in  a  recent  2)aper  on  the  subject,  rest 
and  the  avoidance  of  all  friction  is  advocated."  Dr.  Meyer  L. 
Rhein- in  introducing  the  "Prophylactic  Toothbrush"  to  the 
profession,  says,  in  his  article  on  "  Oral  Hygiene,"  each  brush 
comes  inclosed  in  ;ui  envelope,  upon  which  are  printed  directions 
for  the  intelligent  use  thereof,  and  the  following  caution  :  "  Never 
pass  the  brush  aci'oss  the  teeth,  as  this  movement  destroys  the 
delicate  membrane  wliicli  attaches  the  gum  to  the  teeth,  causing 
recession  of  the  gum,  and  ultimate  loosening  and  loss  of  the 
teeth."  Citations  of  this  could  be  multiplied,  showing  the  gen- 
eral impression  is  that  the  gums  should  not  be  stimulated  to  any 
great  extent ;  that  the  finger,  a  soft  cloth,  or  a  very  soft  tooth- 
brush alone  should  be  employed.  The  use  of  the  finger  is  a 
superstition  which  is  handed  down  from  generation  to  generation 
without  the  slightest  critical  analysis.  If  the  advocate  of  this 
use  would  try  the  exj^eriment,  he  would  see  how  impossible  it 
would  be  to  bring  it  in  contact  Avith  all  the  tissues  of  the  mouth 
that  are  involved  in  this  disease ;  were  it  i^ossible,  the  fingers, 
cloth  and  soft  toothbrush  would  not  accomplish  the  desired 
result. 

Xo  In-usli  should  l)e  used  whose  l)ristles  are  softer  than  the 
medium  ;  very  often  these,  used  once  or  twice  and  dipped  into 
water  or  mouth  washes,  become  so  soft  as  to  be  wholly  unfit  for 
use.  It  is  always  a  good  plan  to  have  two  brushes  to  be  used  on 
alternate  days.  In  this  way  one  can  dry  while  the  other  is  being 
used.  The  general  opinion  has  been  that  friction  u^ion  the  gums 
was  detrimental  on  account  of  the  resultant  tendency  to  absorj;)- 
tion  of  the  gums.  While  this  may  exceiJtionally  be  true,  it  is 
not  true  of  a  majority.  Should  milk,  arsenic,  iron,  strychnine  or 
quinine  be  entirely  abolished  as  remedies  because  occasionally  a 
person  presents  untoward  effects  ?  If  the  alveolar  jn'ocess  be 
very  thin  over  tlie  roots  (if  the  tcetli,  especially  the  cuspids,  the 

'  Dental  Surgery,  imge,  704. 

-New  England  Journal  of  Dentistry,  October,  1884. 


176  INTERSTITIAL    GINGIVITIS. 

patient  must  be  instructed  so  to  use  the  brush  as  not  to  over- 
stimulate  these  particular  parts.  In  such  cases  the  inner  alveolar 
process  and  gum  tissue  may  be  stimulated  with  impunity  and 
with  the  hardest  brush.  Again,  if  the  chronic  interstitial  gingi- 
vitis be  of  long  standing,  or  even  if  chronic  gingivitis  has 
been  jsresent  for  some  time,  stimulation  of  the  brush  will 
cause  the  gums  and  mucous  membrane  to  recede  until  hard, 
sound,  healthy  structure  has  been  secured.  Then  absorption 
will  cease.  In  most  cases  absorption  and  contraction  of  the  gum 
tissue  will  take  place  to  a  more  or  less  marked  degree.  If 
absorption  of  the  alveolar  process  has  taken  place  and  the  gums 
are  puffy,  red  and  swollen,  a  disease  exists  to  be  cured,  regardless 
of  consequences.  The  alveolar  process  and  gums  will  never 
return  to  their  original  position,  but  it  is  a  decided  advantage  to 
have  a  healthy  mouth,  even  if  the  alveolar  process  and  gums 
have  slightly  receded. 

I  have  used  medium  and  stiff  brushes  in  my  practice  for  the 
last  fifteen  years  and  have  failed  to  see  any  ill  results.  For  the 
past  four  years  I  have  made  constant  experiments,  with  the  view 
of  securing  the  proper  shape  and  stiffness  of  the  bristles  and  have 
obtained  uniform  results  in  gum  treatment. 

Proper  employment  of  the  "  gum  massage  brush  "  requires  skill. 
Every  dentist  should  train  his  patient  in  the  method  of  using  the 
brush.  The  gingival  borders  should  not  only  be  stimulated,  but 
the  bristles  should  be  so  jiassed  in  between  the  gum  margin  and 
the  tooth  as  to  remove  the  debris  and  exfoliated  epithelial  scales 
which  have  accumulated  therein.  These  are  often  the  cause  of 
the  irritation.  Unless  this  be  done  the  gum  or  epithelial  tissue 
cannot  perform  its  functions  or  be  restored  to  health.  Stimulat- 
ing astringents  and  germicidal  mouth  washes  should  be  employed 
whenever  the  gums  are  massaged.  The  massage  should  be  done 
three  times  a  day.  The  j)atient  should  be  under  the  care  of  the 
dentist  at  least  twice  or  thrice  a  week,  so  that  he  may  direct  the 
treatment.  If  the  teeth  are  irregular,  care  and  ^^atience  are 
required  to  reach  the  festoons  between  the  teeth.  After  the  gums 
are  in  perfect  health,  the  patient  should  visit  his  dentist  at  least 
four  times  a  year  for  further  instruction.  If  on  inspection  the 
gums  be  found  diseased  at  any  point,  the  dentist  can  direct  the 
attention  of  the  ^^atient  to  the  particular  locality  and  the  disease 


TREATMENT.  177 

l)e  ei-adicatecl.  By  this  inetliod  and  this  alone  can  tlie  gnms  be 
kejit  in  a  healthy  condition.  Each  jiatient  must  be  given  si^ecific 
directions  as  to  the  treatment  of  his  or  Iier  case. 

If  the  gums  have  become  swollen  and  engorged  with  blood 
a  different  method  must  be  employed.  Here  the  absolute  law  of 
medicine  obtains  — "  reiuove  the  cause,"  no  matter  whether  of 
local  or  constitutional  origin.  If  due  to  improper  articulation 
this  must  be  corrected.  If  constitutional,  and  due  to  any  of  the 
mineral  poisons  or  scurvy,  the  system  should  be  flooded  with  large 
quantities  of  pure  water.  There  is  nothing  better  to  rid  the  sys- 
tem of  poisons  and  imj^urities  than  flushing  the  blood  with  from 
threeto  five  quarts  of  pure  water  a  day.  Cathartics  should  be 
employed.  A  Turkish  bath  should  be  used  to  open  the  pores  of 
the  skin,  at  which  time  the  masseur  should  be  instructed  to  stim- 
ulate the  liver,  kidneys,  skin  and  peripheral  nerves.  If  the 
patient  suffer  from  disease  like  syi^hilis,  tuberculosis,  diabetes, 
Bright's  disease,  colds,  including  catarrh,  nervous  prostration, 
antiemia,  etc.,  special  treatment  is  indicated.  Kemove  all  deposits 
and  other  irritants  from  around  the  teeth. 

Two  decades  ago,  I  advocated  the  use  of  the  following  set  of 
scalers ;  nothing  better  has  been  produced  since.  -They  consist 
of  handles,  shanks  bent  at  different  angles,  and  blades  three- 
cornered,  so  that  they  can  be  used  in  three  directions  without 
removing  the  fingers  from  the  tooth  (Fig.  70).  These  are  all 
delicately  made,  and  tempered  very  hard.  Sharp  edges  are 
there  retained.  They  will  reach  every  point  where  tartar  can 
collect.  After  the  dejsosits  have  been  fairly  well  removed,  the 
gums  may  be  syringed  with  hot  water  (Cravens)  to  remove  all 
debris.  The  gums  should  be  saturated  with  tincture  of  iodin 
(U.  S.  P.)  or  iodin  and  aconite,  in  the  following  manner  :  Have  a 
nund)er  of  wooden  toothpicks  (Portuguese  preferable)  wound  with 
cotton,  and  kept  in  a  little  box.  Saturate  the  cotton  and  paint 
the  gum  as  far  as  it  will  go.  Throw  this  into  the  waste  l)asket 
and  take  another,  and  so  on  until  the  gums  are  well  saturated. 
From  three  to  five  picks  will  be  required.  The  assistant  can 
keep  these  in  order  between  patients.  In  such  cases  a  ditt'erent 
massage  brush  is  to  be  used.  One  is  here  required  that  will  so 
lacerate  and  stimulate  the  gums  as  to  relieve  the  congestions. 
This  brush,  made  of  coarser  andstifter  bristles,  should  be  used  like 


178 


INTERSTITIAL    GINGIVITIS. 


the  otlier.  After  two  or  three  days  the  gums  will  contract,  and 
healthy  circulation  follow.  Pain  will  now  be  experienced  in  the 
gums.  The  massage  must  still  be  kept  up.  An  astringent, 
stimulating  and  general  mouth  wash,  should  be  used  in  connec- 
tion with  the  massage.  The  patient  should  return  every  other 
day  for  further  treatment  with  the  iodin,  or  iodin  and  aconite 
used  as  before.  To  reach  an  inflammation,  chronic  and  deep- 
seated,  extending  into  the  peridental  membrane,  periosteum  and 
alveolar  jDrocess,  there  is  nothing  in  medicine  better  than  iodin, 
or  iodin  and  aconite.  This,  and  this  alone,  will  reach  the  deeper 
inflammation.  After  a  few  treatments  and  constant  use  of  the 
massage  brush,  the  gums  will  contract,  and  other  deposits  which 


Fig.  70. 


were  overlooked  at  the  first  sitting  will  now  be  presented  to 
view.  If  the  gums  be  very  painful  at  the  first  sitting,  no  effort 
should  be  made  to  remove  the  deposits  until  the  inflammation 
has,  in  a  measure,  subsided.  The  iodin  treatment  and  massage 
should  be  conducted  as  suggested  until  the  gums  have  been 
reduced  and  the  pain  ceases.  After  they  have  been  restored  to 
health,  constant  massage  with  the  medium  brush  must  be 
employed  two  or  three  times  a  day .  The  patient  should  return 
to  the  dentist  as  often  as  necessary  (every  month  or  two)  to 
have  the  gums  examined,  and  for  further  direction. 


TREATMENT.  179 

As  has  been  already  shown,  chronic  interstitial  gingivitis  may 
extend  only  to  the  peridental  membrane,  to  the  periostenm,  or  it 
may  extend  throughont  the  alveolar  process  with  the  absorjition 
of  the  bone  the  entire  length  of  the  root  of  the  tooth.  Pns 
infection  and  serumal  deposit  may  or  may  not  take  place.  In 
the  early  stages  of  this  progressive  inflammation,  the  first  is  prob- 
able. If  pus  and  deposits  are  present  they  can  be  treated  with 
signal  success  according  to  the  symptoms  and  as  hereinafter 
explained.  As  already  suggested,  the  gum  massage  brush  must 
be  vigorously  used  to  relieve  the  engorged  tissues  of  blood. 
Since  absorption  of  the  alveolar  process  depends  upon  irritation 
and  inflammation,  this  must  be  removed  as  quickly  as  possible. 

In  the  treatment  of  deep-seated  interstitial  inflammation, 
iodin  or  iodin  and  aconite  has  always  been  regarded  by  physi- 
cians and  surgeons  as  the  best  remedy.  The  gums  should  be 
thoroughly  saturated  twice  or  thrice  weekly,  as  already  suggested. 
If  the  alveolar  process  be  so  absorbed  that  the  tooth  has  become 
loose,  the  case  is  hopeless.  In  such  unstable  tissues,  especially 
when  inflammation  extends  through  the  process  and  lacunar, 
perforating  canal  absorption  and  halisteresis  is  going  on,  reversal 
of  the  order  so  as  to  set  the  osteoblasts  to  tissue-building  is 
hardly  to  be  expected.  The  tendency  is  to  destroy  and  not 
restore  the  alveolar  process.  In  such  cases  the  tooth  must  be 
fastened  to  the  other  teeth  perfectly  tight  to  prevent  motion  in 
any  direction.  The  movement  of  the  tooth  in  mastication  inten- 
sifies the  irritation,  which  in  time  only  increases  the  absorption. 
Liberal  use  of  iodin  or  iodin  and  aconite  and  the  gum  massage 
brush  is  all  that  can  be  done  to  reduce  the  inflammation  and 
absorption  as  nuich  as  possi1:)le.  The  exfoliation  is  only  a  matter 
of  time.  If  the  tootli  or  teeth  cannot  be  retained  perfectly  tight, 
no  matter  how  healthy  the  surrounding  tissues  may  be  restored, 
the  irritation  produced  by  the  loose  teeth  will  soon  set  up  inflam- 
mation in  the  surrounding  tissues.  The  sooner  the  loose  teeth 
are  removed  the  better.  In  no  case  can  the  bone  tissue  be 
restored,  if  the  matrix  or  cartilage  be  destroyed,  since  in  this  tlie 
osteoblasts  are  located.  If  the  matrix  or  cartilage  be  destroyed, 
a  fibrous  union  (such  as  occurs  in  the  case  of  implanted  teeth  and 
the  imbedding  of  foreign  bodies  in  the  tissues  of  the  body)  only 
is  possible. 

13 


180 


INTERSTITIAL    GINGIVITIS. 


If  inflammation  have  extended  into  the  j^eriosteum,  peri- 
dental membrane  and  alveohir  ^^rocess,  serumal  calculi  are  fre- 
quently dejDosited  upon  the  roots  of  the  teeth.  When  this  has 
taken  jilace,  the  calculus  must  be  removed.  This  should  be 
done  with  the  utmost  care,  in  order  that  adjacent  tissues  may  not 
be  injured,  or  inflamed  parts  infected  with  pus  germs.  Since 
dead  bone  is  not  present,  the  ojjerator  should  confine  his  instru- 
mentation entirely  to  the  root  or  roots  of  the  teeth,  with  as  little 
injury  as  possible  to  the  adjacent  tissues.  The  alveolar  process 
must  under  no  consideration  be  touched.  Riggs  believed  that 
the  edge  of  the  alveolar  process  was  always  in  a  state  of  dis- 
integration, and  that  it  should  be  so  scraped  as  to  get  a  fresh 
surface,  on  the  principle  of  caries  of  bone.  Many  dentists  are 
oj^erating  in  this  manner  at  the  present  time.  I  have  elsewhere 
shown  simj)le  absorption  and  not  caries  is  present.     Such  treat- 


FiG.  71. 

ment  is  wholly  unnecessary  and  contraindicated.  The  object  of 
the  removal  is  to  allow  the  fibrous  tissue  of  the  peridental  mem- 
brane, (after  health  is  restored)  to  tighten  about  the  root,  which 
cannot  be  accomplished  when  foreign  substances  are  present. 
Pushing  instruments  must  never  be  used,  but  only  such  instru- 
ments as  have  smooth  and  round  backs,  temjDered  very  hard  so  as 
to  retain  sharp  edges.  These  instruments  should  be  small,  with 
small  points  to  reach  depressions,  and  to  be  as  universal  as  jjos- 
sible.  Such  an  instrument  is  to  be- found  in  the  spoon  excavator 
(Fig.  71).  The  shank  can  be  bent  to  suit  the  oiDcrator.  This  is 
to  be  carried  gently  along  the  length  of  the  root  and  passed 
oyer  the  deposit  with  a  firm  liand,  resting  the  finger  upon  some 
other  teeth.  The  drawing  motion  is  invariably  to  be  from  the 
membrane,  and  toward  the  crown.     The  deposits  are  scaled  off" 


TREATMENT.  181 

painleSusly.  The  round  blade  being  larger  than  the  shank,  and 
cutting  upon  three  edges,  lialf  of  the  root  in  both  directions  can 
be  circled  without  removing  the  instrument.  A  similar  instru- 
ment bent  at  the  shank  in  tlie  opposite  direction  may  be  used  on 
the  other  side.  After  all  of  the  roots  of  the  teeth  have  been 
scaled,  the  spaces  are  to  be  syringed  out  with  warm  or  liot 
water  (Cravens).  The  gums  are  to  be  thoroughly  saturated 
inside  and  out  with  iodin.  The  gum  massage  brush  is  to  be  used 
thrice  daily  as  before.  The  patient  should  return  twice  or  thrice 
a  week  for  further  instructions.  The  contracting  gums  will 
assist  greatly  in  revealing  the  deposit.  If  deposits  still  remain 
on  the  roots  (the  appearance  of  the  gums  will  indicate  its  pres- 
ence) further  use  of  the  scalers  is  indicated.  The  delicate  instru- 
ments and  the  accustomed  sense  of  touch  will  reveal  the  hidden 
calculus. 

With  the  precautions  already  noted,  local  anaesthesia  is 
unnecessary.  The  smooth,  round  surfece  of  the  back  of  the 
instrument,  if  carefully  inserted,  will  not  produce  pain. 

If  the  gum  be  painful  to  the  touch,  or  if  the  patient  be 
nervous  and  sensitive,  application  of  tincture  iodin  may  be  used, 
together  with  massage,  for  a  few  days  before  scaling  is  resorted 
to.  The  sensitiveness  will  soon  disapjDear,  when  the  instrument 
may  be  inserted  without  difficulty. 

A  feAv  years  hence,  the  profession  will  regard  a  dentist  whose 
patients  have  pus  oozing  from  the  gums  as  a  i^rehistoric  relic  and 
the  patient  as  an  individual  wliose  filth  provokes  the  contempt  of 
his  fellows.  In  this  day  of  antisepsis,  the  dentist  is  as  account- 
able for  pus  infection  of  his  patients  as  the  physician  or  surgeon. 

There  is  no  more  excuse  for  the  dentist's  patient  being  in- 
fected than  the  surgeon's.  If  ordinary  antiseptic  precautions  are 
taken,  pus  infection  will  not  often  occur.  Prevent  inflammation 
of  the  gum  margin  and  pus  infection  cannot  follow,  no  matter 
how  many  germs  be  in  the  mouth.  This  is  an  absolute  law  of 
general  pathology.  It  has  been  proven  by  the  experiments  made 
by  Miller,  G.  T.  Carpenter  and  myself  on  dogs,  rabbits  and  man. 

Tbe  illustrations  of  the  progress  of  interstitial  gingivitis  teach 
that  only  the  mildest  treatment  is  indicated.  Harsh  treatment 
on  the  inflamed  bone  or  fibrous  tissue,  either  with  instruments  or 
ilrugs,  nuist   not   be   employed.     Heroic  treatment,  such   as  the 


182  INTEE8TITIAL    GINGIVITIS. 

indiscriminate  application  of  suli3hnric  and  lactic  acid  and  sim- 
ilar drugs  in  nearly  or  quite  full  strength,  is  not  justified  by  the 
surgical  princij)les  of  today.  No  surgeon  would  think  of  making 
such  an  application  to  inflamed  bone  in  other  parts  of  the  body 
without  he  wished  necrosis  with  a  desired  sequestrum.  INIuch 
less  would  the  intelligent  operator  use  such  treatment  in  a  transi- 
tory structure  which  predisposed  to  destruction.  In  a  number  of 
instances  exfoliation  of  the  anterior  plate  of  the  alveolar  process 
has  resulted  from  this  treatment,  to  say  nothing  of  the  intense 
pain  produced.  J.  M.  Whitney'  has  had  four  cases  in  his  prac- 
tice in  which  serious  results  followed.  The  first  indication  is  to 
remove  the  cause.  Instrumentation  should  be  resorted  to  only 
to  remove  tartar  and  calcic  deposits.  This  must  be  done  in  such 
a  manner  as  not  to  infect  the  deeper  inflamed  tissue  6r  carry  the 
products  of  inflammation  into  healthy  tissue.  The  treatment  of 
infected  tissue  within  and  about  the  alveoli  is  not  unlike  treatment 
of  abscesses  and  ulceration  elsewhere.  Such  drugs  as  are  used 
in  abscesses  and  ulcers  in  other  tissues  are  indicated  here  in  the 
same  strength.  If  strong  drugs  be  used  they  should  not  be  per- 
mitted to  remain  in  the  tissue,  lest  necrosis  of  the  alveolar  process 
occur.  They  must  be  diluted  or  removed  altogether  after  they 
Irave  accomplished  their  purpose.  Very  serious  results  have 
occurred  from  careless  use  of  drugs.  When  abscesses  have 
formed  they  should  be  opened  and  hydrogen  peroxid  —  or,  which 
has  answered  my  purpose  equally  well,  hot  water  (Cravens)  —  is  all 
that  is  necessary.  More  difficult  is  treatment  of  ulceration  of  the 
tissue  near  the  root  of  the  tooth.  Ordinary  cases  will  heal  after 
hot  water  or  hydrogen  peroxid  have  been  applied.  In  some 
cases  the  pus  germs  have  followed  the  inflammation  along  the 
course  of  the  vessels  quite  a  distance  into  the  interstitial  tissue. 
In  such  cases  they  are  difiicult  to  reach.  A  small  syringe 
(George  T.  Carpenter's)  may  be  employed,  or  the  drug  may  be 
carried  to  the  part  on  the  end  of  a  long,  thin  orange-wood  stick. 
In  all  cases  the  drug  must  be  directly  applied  to  the  part  in  order 
to  have  beneficial  results.  Applications  of  iodin  should  be  used, 
as  already  suggested.  Iodin  carried  to  the  ulcerated  surface  often 
suffices  to  destroy  the  pus  secretion.  Ordinarily  one  or  two 
applications  is  sufficient.    Occasionally  calcic  deposits  are  located 

'  International  Dental  Journal,  April,  1899. 


TREATMENT.  183 

in  front  of  the  infected  surface  and  the  drug  does  not  i-eacli  the 
part.  In  such  cases  the  deposit  must  be  removed.  If  the  pus  do 
not  cease  at  the  first,  second  or  even  third  application,  this  is  not 
because  tlie  drug  is  not  sufficiently  strong,  but  because  it  does  not 
reach  the  infected  part.  Continued  applications  of  iodin  exter- 
nally and  internally,  carried  well  up  between  the  roots  of  the 
tooth  and  the  alveolar  jjrocess  will,  in  time,  produce  the  desired 
result.  When  pus  ceases  to  flow,  antiseptic  treatment  must  stop. 
The  iodin  and  massage  treatment  nnist  then  be  pushed  until  the 
interstitial  inflammation  has  been  reduced  and  the  gums  con- 
tracted tightly  about  the  necks  of  the  teeth. 

After  the  tissues  have  been  placed  in  a  healthy  condition, 
they  Avill  require  the  constant  attention  of  the  operator,  since, 
like  other  tissues  of  the  body  when  once  diseased,  favorable  con- 
ditions will  cause  a  recurrence.  The  patient  must  return  to  the 
operator  frequently  so  that  he  can  advise  as  to  the  use  of  massage. 

I  have  elsewhere  shown  that  uric  acid  (like  lactic  and  other 
acids,  mercury,  lead  and  brass  poisoning)  may  produce  local 
irritation  in  a  small  number  of  cases,  resulting  in  interstitial 
gingivitis.  Uric  acid  is  absorbed  into  the  blood  and  is  thus  car- 
ried to  all  parts  of  the  body.  As  mercury,  lead,  brass  and  potas- 
sium iodide  collect  in  the  tissues  of  the  alveolar  process,  on 
account  of  the  sluggish  blood  supply,  so  does  uric  acid,  setting- 
up  inflammation.  These  cases  are  easily  diagnosed,  since,  unlike 
the  ninety-four  per  cent  of  cases  that  begin  at  the  gum  margin 
without  pain  and  are  of  long  standing,  these  set  up  a  spontaneous 
inflammation  in  an  otherwise  healthy  alveolar  process.  This 
may  occur  about  one  tooth,  or  more  may  be  involved  ;  usually  it 
involves  the  tooth  or  teeth  standing  alone  or  having  improper  or 
no  articulation.  The  inflammation  is  followed  liy  acute  pain. 
If  this  be  not  reduced  an  abscess  may,  as  elsewhere  shown,  form 
at  some  locality  about  the  alveolar  process.  Inflammation  will 
extend  throughout  the  alveolar  process  and  rapitl  al>sorption 
result.  The  tootji  will  loosen  in  the  socket.  If  systemic  treat- 
ment be  not  at  once  instituted,  exfoliation  of  the  tooth  or  teeth 
shortly  ensues.  The  first  thing  indicated  in  sui-li  cases  is  an 
a]iplication  of  iodin  to  reduce  inflannnation  and  pain.  The  urine 
for  twenty-four  hours  should  be  secured  for  chemical  analysis. 

The  materials  and    appliances  necessary  for  the  ])urpose  of 


184  INTERSTITIAL    GINGIVITIS. 

making  an  examination  of  the  urine  for  uric  acid  are  many  and 
the  method  requires  considerable  time.  The  dentist  can  do  the 
work,  but  it  will  be  much  more  satisfactory  (if  he  must  know  the 
quantity  eliminated  each  day)  to  send  it  to  a  competent  chemist. 
Should  he  desire  to  make  the  urine  analysis,  I  should  recom- 
mend the  method  suggested  by  Bartley  ^  in  which  he  says,  "  The 
estimation  of  uric  acid  is  usually  attended  with  much  difficulty 
and  consumption  of  time.  The  author  has  devised  the  following 
volumetric  method,  which  is  fairly  rapid,  reasonably  accurate 
and  requires  little  skill.  It  can  therefore  claim  a  ])\nce  as  a 
clinical  method.  The  process  is  based  upon  the  well-known 
fact  that  uric  acid  is  completely  precij)itated  from  its  solutions 
containing  an  excess  of  ammonium-magnesium  mixture  and 
ammonium  hydroxide,  by  silver  nitrate.  When  the  precipita- 
tion is  complete,  the  slightest  trace  of  silver  in  solution  is  shown 
by  the  dark  color  produced  in  a  droj)  of  the  clear  solution  by  a 
soluble  sulphide."  The  method  of  procedure  is  thus  explained, 
should  the  uric  acid  excreted  in  twenty-four  hours  be  less  than  .8 
grams  or  10.8  grains  it  is  safe  to  say  that  it  is  retained  in  the 
system. 

Imperfect  tissue  metabolism,  as  V.  A.  Gudex,"  of  Milwaukee, 
has  shown,  results  in  the  formation  of  the  following  acids  and 
substances :  uric,  hippuric,  oxaluric,  carbonic,  lactic  and  lac- 
tates, caprylic,  caproic,  valerianic,  butyric,  propionic,  acetic, 
stearic,  oleic,  palmitic,  formic,  cholalic,  tuarilic,  damaluric, 
damalic,  and  suceimic  acids.  Of  these,  the  uric  acid  seems  to  act 
least  as  an  irritant.  The  urine,  therefore,  should  be  examined 
for  general  acidity,  the  general  treatment  of  which  will  accom- 
plish all  that  is  to  be  desired.  A  safe  and  delicate  test  can  be 
accomplished  by  determining  the  alkalinity  of  the  urine,  saliva, 
perspiration,  expectoration  and  dejection.  The  dentist  is  fortu- 
nate in  this  because  he  has  every  convenience  at  hand.  Lieb- 
reich's  methods  of  the  use  of  plaster  of  paris  plates  as  elaborated 
by  A.  H.  Hoy,^  of  Chicago,  is  most  admirably  adapted  for  this 
purpose,  since  the  test  can  be  readily  ap^jlied.  To  make  the 
plates,  mix  a  very  thin  quantity  of  dental  plaster  to  the  con- 


'  Medical  Chemistry,  page  641 ;  fifth  edition. 
2  Items  of  Interest,  May,  1899. 
^Eating  and  Drinking. 


TEEATMENT.  ]  85 

sistency  of  cream,  care  being  taken  to  thoroughly  incorjiorate 
the  plaster.  Take  two  panes  of  window  glass,  cut  four  j^ieces  of 
wood  three-sixteenths  of  an  inch  in  thickness  and  j^lfice  one  at 
each  corner  of  the  glass ;  now  pour  the  plaster  into  the  center, 
place  the  other  plate  of  glass  above  and  press  it  down  upon  the 
blocks  of  wood.  By  this  method  a  very  smooth  surface  can  be 
obtained.  Make  a  round  cutter  out  of  tin,  the  size  of  a  twenty- 
five  cent  piece.  Remove  the  upper  piece  by  sliding  it  off,  cut 
out  round  disks  just  before  the  plaster  hardens.  These  are  pre- 
pared in  the  following  manner:  A  solution  of  litmus  in  12 
parts  of  water  is  rendered  alkaline  or  bright  blue  by  adding  a 
few  drops  of  aqua  ammonia.  After  the  disks  have  become  per- 
fectly hard,  the  smooth  polished  surface  is  to  be  painted  with 
the  solution,  using  a  camel's-hair  brush.  Two  or  three  apj^lica- 
tions  are  to  be  made,  until  an  even  blue  stain  is  obtained.  Have 
a  solution  of  chemically  pure  sulphuric  acid,  two  j)arts  in  five 
hundred  of  distilled  water,  ready  in  a  bottle,  and  a  bottle  of  dis- 
tilled water.  To  prepare  the  disk  for  the  test,  scrape  one-half 
of  the  dark  blue  surface  of  the  plate  until  a  slight  blue  sur- 
face is  obtained.  This  requires  the  removal  of  only  a  slight 
amount,  since  the  blue  stain  only  j)enetrates  a  short  dis- 
tance. With  a  small  brush,  dipped  into  the  acid,  draw  it  quickly 
over  the  surface  exposed,  giving  a  red  appearance  to  the  field 
adjoining  the  blue.^  A  bit  of  cotton,  wound  around  the  end 
of  a  toothpick  wet  with  distilled  water  and  applied  to  the 
two  colors,  will  produce  no  change,  thus  proving  everything  to 
be  in  working  order.  The  fluid  to  be  tested  —  urine,  saliva  or 
perspiration  —  may  noAV  be  applied.  When  possible,  the  exudate 
must  be  applied  to  the  test  as  soon  as  it  leaves  the  body,  care 
being  taken  to  apply  a  fixed  amount  each  time.  Apj^ly  the 
fluid  to  be  examined  to  both  the  blue  and  red  fields.  When 
saliva  is  used,  the  mouth  must  be  rinsed  two  or  three  times  and 
the  quantity  first  sucked  out  of  the  ducts  must  not  be  used. 
Fresh  saliva  direct  from  the  glands  should  only  be  used.  The 
plates,  after  they  have  been  used,  may  be  re-stained  and  used 
indefinitely.  The  dentist  should  make  repeated  tests  of  the 
secretions    of    healthy    individuals    under    different    conditions 


'It  is  almost  impossible  to  obtain  a  satisfactory  permanent  red  litmus.    By  this 
method  the  red  and  blue  fields  stand  out  in  bold  contrast. 


186  IXTEE8TITIAL    GINGIVITIS. 

before  studying  tliose  of  diseased  conditions.  This  method  is 
a  more  delicate  test  than  it  is  j)0ssible  to  make  even  with 
litmus  paper.  Litmus  paper  often  fails  to  reveal  reaction, 
which  will  be  most  obvious  by  this  method. 

The  secretions  of  the  body,  if  found  to  be  acid,  must  be 
placed  in  an  amphoteric  condition  as  soon  as  possible.  An 
amphoteric  condition  is  a  reaction  of  the  urine,  by  which 
both  the  blue  and  the  red  litmus  are  affected.  If  the  red 
becomes  blue  and  the  blue  red  it  indicates  that  there  is  an 
amphoteric  reaction.  The  salt  giving  the  alkaline  reaction  is 
the  trisodic  phosjjhate ;  that  giving  the  acid  reaction  is  the  mon- 
asodic  j^hosphate.  When  a  uniform  color  is  produced  it  shows 
that  tlie  alkaline  iand  acid  salts  are  being  properly  excreted  in 
proi^er  amounts  with  no  excess  of  free  acid. 

The  normal  urine  sjjecific  gravity  is  1018  to  1025.  To 
determine  the  specific  gravity  the  morning  urine  should  be  used. 
If  about  1018  or  lower  and  acid,  it  is  due  to  fermentation  in 
small  intestines.  In  such  cases  avoid  yeast  bread,  acid  fruits, 
wines,  vinegar  and  all  acids.  If  specific  gravity  is  1025  or 
more  and  acid,  avoid  meats.  From  five  to  seven  pints  of  pure 
water  should  be  taken  each  day,  to  flush  the  blood  and  kidneys 
and  thus  cleanse  the  system.  Certain  patients,  especially  neu- 
rasthenics, nervous  dyspeptics  and  many  lithasmics,  have  a 
repulsion  to  pure  water.  The  water  can  be  adjusted  to  these 
idiosyncrasies  by  the  employment  of  lithia  or  other  effervescent 
tablets.  The  main  object  is  to  preserve  in  such  cases  the  promi- 
nent idea  of  the  water  being  medicated.  Local  treatment,  as 
elsewhere  described,  should  here  be  resorted  to.  Besides  the  use 
of  water,  dietetics  in  dentistry  involve  chiefly  a  conservative 
question. 

-  Under  most  conditions  of  suboxidation  and  imperfect  elimi- 
nation, as  elsewhere  shown,  the  gums  are  forced  to  assume  an 
excretory  energy  to  which  they  are  unequal.  As  a  consequence 
a  foundation  is  laid  for  interstitial  gingivitis,  which,  in  all  of  its 
types,  may  seriously  threaten  tlie  integrity  of  the  teeth.  Nay, 
more,  by  furnishing  a  culture  medium  for  pus  microbes  it  may 
threaten  the  general  health,  not  only  through  systemic  infec- 
tion, but  also  through  its  interference  with  proper  gastro-intestinal 
dio'estion.     Amono;  the  restrictions  in  diet  which  dental  hv2;iene 


TREATMENT.  187 

demands  is,  first,  a  restriction  in  foods  and  water  containing  an 
excess  of  lime  salts,  which  produce  tartar.  As  excess  of  foods 
containing  nitrogen,  when  aided  by  an  imperfect  assimilation  of 
the  carbohydrates,  tend  to  produce  constitutional  conditions  like 
lithsemia,  gout,  etc.,  which  affect  tissue  nutrition  of  the  gums,  these 
foods  require  restriction  and  adaptation  to  the  particular  ease. 
While  the  constitutional  condition  underlying  lithaemia  markedly 
predisposes  to  gum  irritations  and  inflammations,  its  value  as  an 
exciting  cause  is  but  slight.  Lactic  acid,  as  has  been  elsewhere 
]iointed  out,  is  a  more  marked  local  excitant.  In  the  constitutional 
production  of  lactic  acid,  ingestion  of  the  carbohydrates  without 
assimilation  plays  a  part.  Scurvy,  which  may  seriously  threaten 
the  integrity  of  the  gums,  requires  the  usual  dietetic  treatment. 
While  there  are  indications  of  the  untoward  effects  of  infantile 
scurv}^  on  the  gums,  the  pathology  and  consequences  of  it  are 
not  as  well  known  as  those  of  scurvy  in  the  adult.  The 
researches  on  scurvy  in  the  infant  tend  to  show  that  it  results 
from  a  monotony  of  diet  rather  than  the  absence  of  any  article  of 
diet.  The  dietetics  of  dentistry,  therefore,  involve  precisely  the 
same  princi2)les  as  do  the  treatment  of  the  constitutional  con- 
ditions which  are  the  predisposing  factors  of  the  gum  disorders. 
During  the  entire  process  of  treatment  (indeed  before  the 
treatment  begins)  a  suitable  mouth  wash  should  be  used  two  or 
three  times  a  day.  This  should  be  composed  of  a  germit'ide, 
antiseptic  disinfectant  and  deodorant,  and  should  be  used  at  the 
time  of  the  massage. 


INDEX  OF  AUTHORS. 


PAGE 

Alexander,  H.  C.  B 145 

Allbright         3 

Andrews,  R.  R 89 

Arcovy 4 

Barlow,  Thomas 95 

Barrett 174 

Bartley 184 

Black     .     5,  34,  41,  47,  48,  51,  53,  56,    98 

Beodecker 174 

Bondurant 91 

Bonwill 2,  157 

Brown 2 

Brubaker,  A.  B 68 

Buzzard 97 

Calve,  Marshall  de 2 

Carpenter,  G.  T.  125,  165,  170, 

181,  182 

Cartright,  Hamilton 4 

Clowes 3 

Coles,  Oakley 4 

Collins,  J 66 

Congdon 68 

Cravens 181,  182 

Cruveilier,  C 92 

Dana,  C.  L 97 

Dickinson,  Howship 78 

Ebner,  Von    ....   5ri,  153,  158,  160 

Eisenhart 159 

Enderlin    . 76 

Essig,  C.  J 3 

Evans,  W.  A. 123 

Farrar,  F.  N 4 

Fitzgerald 9,  68,  167 

Flower,  Alsop 14 

Foster        11 

Fuchard,  H.  A 2 

Galippe      .     .       4,12,122,123,124,151 

Geddings,  H.  D 75 

Gray .37 

Gudex,  V.  A 184 

Hektoen,  L 127,  155 

Hertwig,  0 56,  146 

Herzog,  M 124 


PAGE 

Hirt 97 

Hogben 94 

Howell 77 

Hoy,  A.  H.     ........  184 

Ingersol,  L.  C 4 

Izklai,  Joseph 4 

Jacobi 95 

Jacobson 75 

Joirac 2 

Jourdain 2 

Kaecker 2 

Ivaufmann       61,  154,  157,  158 

Kirk 12,  68 

Koch 12,  151 

Kolliker     ....       30,33,56,62,161 

Kuttner 169 

Magitot      .     .     .  2,  7,  53,  55,  57,  58,  91 

Mailhol 11 

Malasses 4 

Malenfant 79 

Miller   .     .       8,  cS2,  89,  122,  123,  125,  181 

Mills 3 

Minot         42,  53,  56,  146 

Morgan,  de 31 

Niles,  N.  S 3 

Noyes,  Frederick 48 

Patterson        4,  6,  8,  89 

Pedley 6,  7 

Pierce,  C.N.    .     .     .       8,  12,  .37,. 08,  96 

Quain         10,  11 

Rawls,  A.  0 4,  95 

Rechlinghausen,  Von 159 

Reese 4 

Reeves 68 

Rehwinkle 3 

Rhein OS,  175 

Riggs,  J.T.      . 2,  180 

Robin 53,  55,  57,  58,  91 

Rokitansky 169 

Rose 54 

Salisbury,  J.  H.        .      .     .       69,71,  79 

Sayre,  Charles  E 14 

Scheff 2 


190 


INDEX    OF    AUTHORS. 


PAGE 

Scheheoetskey 78 

Schmidt,  C 73,  74,  7G,  78 

Serres 47 

Sirletti        3 

Starr,  A.  R 5 

Stevenson 78 

Sudduth,  W.  X.        ...  5,  6,  7,  8,  161 

Sutton,  Bland 7 

Talbot,  E.  S 5,  47 


PAGE 

Tomes        27,  31,  175 

Yolkmann      ...     31,  62,  63,  153,  160 

Virchow 169,  170 

Waldeyer 56 

Walker 4 

Wesener,  J.  A 69,    70 

Whitney,  J.  M 182- 

Zawadsky 7& 

Ziegler 28,  158- 


INDEX  OF  SUBJECTS. 


PAGE 

Acadians,  Teeth  of 1 

Alveolar  Process 21 

Absorption  of 147 

Absorption 157 

Absorption       and        Trophic 

Change        162 

Changes 149 

Dermal  Bones 96 

Germ  Infection    .     .  .     .     96 

Hypertrophy  of 29 

Antimony 144 

Arsenic 144 

Bone  Absorption 59 

Bone  Building 59 

Brass 144 

Interstitial  Gingivitis    .     .     .     94 

Bromides        145 

Calcic  Deposits 168 

Calcospherites 41,  133 

Calculi,  Salivary 78 

Carnivora,  Interstitial  Gingivitis  in  .  14 
Catarrhal  Idiosyncrasy  ....  5 
Cave  Dwellers,  Teeth  of    ...     .       1 

Cementoblasts 42 

Cementoolasts 61 

Children,  Degenerate 89 

Diathetic 89 

Interstitial  Gingivitis  in      .     .     81 

Neurotic 89 

Pyorrhcea  in 89 

Debris,  Epithelial 55 

Dental  Operations  and  Alveolar  Pro- 
cess    150 

and  Bone  Absorption    .      .     .   150 

Dental  Shelf 55,    56 

Degeneracy  and  Degenerate  Tissues  .     87 

Dentitions,  The  Three 84 

Dogs,  Interstitial  Gingivitis  in      .  14,    98 
Mercuric     Interstitial    Gingi- 
vitis in 117 

Pyorrhcea  Alveolaris  in  .  .  98 
Ebner,  Von,  Vessels  of  ....  31 
Egyptians,  Teeth  of 1 


PAGE 

Embryology  of  the  Tooth   ....     46 
Endarteritis  Obliterans       ....   154 
and  Tuberculosis      ....   155 
Exanthemata  and  Catarrhal  Gingi- 
vitis   7 

Follicle,  The  Dental 55 

Gingivitis 5 

Expulsive 11 

Interstitial 9 

and  Pyorrhcea 9 

Glands    of  Mucous   and    Peridental 

Membranes 47 

Greeks,  Teeth  of 1 

Gums 42 

Halisteresis     ....     61,  62,  153,  158 

Haversian  Canals 30 

Heredity 13 

Interstitial  Gingivitis    .     .     .     .10,     12 

Antimony 144 

Arsenic 144 

Atavism  and 83 

Auto-Intoxication  and  ...     66 

Bacteriology  of 122 

Brass 144 

Bromide 145 

Carnivora  in 14 

Causes 12 

Degeneracy  and 86 

Dogs 98 

Environment  and     ....     84 

Heredity  and 83 

Heredity  in 13 

Inorganic  Salts  and       ...     73 

Iodide 145 

Lactic  Acid  and 152 

Mercuric 142 

In  Dogs 117 

Nerve  Phases  of        ....     13 

Pathogeny  of 151 

Plumbic 143 

Pyorrhcea  Alveolaris  and  .  .  162 
Scorbutic  in  IMan  ....  127 
Scurvy  and       .      .      .     13,  65,     94 


192 


INDEX    OF   SUBJECTS. 


PAGE 

Intel  stitial  Gingivitis  — 

Tartar  and 148 

Theories  of 65 

Toxic  Causes  of  .      .     .     .  13,    92 

Treatment 172 

Troplio-Neuroses  and    .      .  66,     92 

Uric  Acid  and 68 

Iodides 145 

Jaw,  Evolution  of    .     .      .     .     .      .149 

Evolutionary  Changes  in    .      .20 
Racial  Changes  in    ....     20 

Lake  Dwellers,  Teeth  of    ...      .       1 

Lactic  Acid   and   Interstitial   Gingi- 
vitis   152 

Lacunar  Absorption       .      .     .     .  62,  153 

Lead 143 

Interstitial  Gingivitis  and  .     .     94 
Locomotor  Ataxia    and    Gum    Dis- 
order        13 

Mercury 142 

Interstitial  Gingivitis  and       .     93 
Mouth  Breathing  and  Catarrhal  Gin- 
givitis      7 

Mucous  Membrane,  Glands  of      .     .     47 

Histology  of 42 

Mucus,  Bactericidal  Function  of  .     .88 

Odontoblasts 42 

Osteoblasts 42 

Osteoclasts 61 

Osteomalacia        ....     62,  146,  159 
Papillary  Layer,  Comparative  Anat- 
omy   47 

Paretic    Dementia    and    Gum    Dis- 
order      ...  13 

Perforating  Canal  Absorption      .  62,  153 
Pericementitis  Phagadenica     ...       5 

Peridental  Membrane 33 

Glands  of 47 

Inflammation 1 

Periosteum 33 

Periostitis  Alveo-Dentalis        ...       2 

Dentalis 2 

Pockets  and  Interstitial  Gingivitis    .   152 


PAGE 

Potassium    lodid    and    Interstitial 

Gingivitis 94 

Pregnancy  and  Osteomalacia  .     .     .   159 

Primitive  Races,  Teeth  of  ...      .       1 

Pyorrhosa  Alveolaris,  Bacteriology  of  162 

Catarrhal  Idiosyncrasy       .     .       5 

Causes  of 2 

Constitutional  Causes  .  3,  4,  5 
Constitutional  Effects  of    .     .   167 

Degeneracy  and 5 

Dogs 98 

Eruptive  Fevers        ....       7 

History 2 

Intestinal  Disorders  from   .      .   167 

Lactic  Acid 8 

Nervous  Causes 3 

Parasites  and "8 

Pathology  of 6,      7 

Syphilis  and 8 

Systemic  Disease  and     ...       8 

Uric  Acid  and 8 

Scurvy 96,  127 

Sodium    Chloride    and    Interstitial 

Gingivitis 95 

Stomatitis  Catarrhalis 6 

Teeth,  Changes  in    .....     .  146 

Changes  in  Position  of  .  .  .28 
Decay  of    ......     .   147 

Embryology  of 146 

Irregularities  of 148 

Periods  of  Evolution  .  .  .  146 
Periods  of  Involution  .  .  .  146 
Trophic  Disorders  of     ...     96 

Third  Molar 149 

Disappearance  of      ....     21 

Tootli  Embryology 42,    53 

Form  Changes 149 

Transitory  Structures    .     .     .     .20,  147 

Tropho-Neuroses 13,    96 

Ulitis U 

Uric  Acid  and  PyoiThosa  Alveolaris  3,      8 
Volkmann's  Canals 31 


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